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1.
Medwave ; 24(3): e2783, 30-04-2024. tab, ilus
Article in English, Spanish | LILACS | ID: biblio-1553773

ABSTRACT

INTRODUCTION: Chronic obstructive pulmonary disease is a systemic disease characterized not only by respiratory symptoms but also by physical deconditioning and muscle weakness. One prominent manifestation of this disease is the decline in respiratory muscle strength. Previous studies have linked the genotypes of insulin-like growth factor 1 and 2 (IGF-1 and IGF-2) to muscle weakness in other populations without this disease. However, there is a notable knowledge gap regarding the biological mechanisms underlying respiratory muscle weakness, particularly the role of IGF-1 and IGF-2 genotypes in this pulmonary disease. Therefore, this study aimed to investigate, for the first time, the association between IGF-1 and IGF-2 genotypes with respiratory muscle strength in individuals with chronic obstructive pulmonary disease. In addition, we analyzed the relationship between oxidative stress, chronic inflammation, and vitamin D with respiratory muscle strength. METHODS: A cross sectional study with 61 individuals with chronic obstructive pulmonary disease. Polymerase chain reaction of gene polymorphisms IGF-1 (rs35767) and IGF-2 (rs3213221) was analyzed. Other variables, related to oxidative stress, inflammation and Vitamin D were dosed from peripheral blood. Maximal inspiratory and expiratory pressure were measured. RESULTS: The genetic polymorphisms were associated with respiratory muscle strength ( 3.0 and 3.5; = 0.57). Specific genotypes of IGF-1 and IGF-2 presented lower maximal inspiratory and expiratory pressure (<0.05 for all). Oxidative stress, inflammatory biomarkers, and vitamin D were not associated with respiratory muscle strength. CONCLUSION: The polymorphisms of IGF-1 and IGF-2 displayed stronger correlations with respiratory muscle strength compared to blood biomarkers in patients with chronic obstructive pulmonary disease. Specific genotypes of IGF-1 and IGF-2 were associated with reduced respiratory muscle strength in this population.


INTRODUCCIÓN: La enfermedad pulmonar obstructiva crónica es una enfermedad sistémica caracterizada no solo por síntomas respiratorios, sino también por el deterioro físico y la debilidad muscular. Una manifestación destacada de esta enfermedad es el declive en la fuerza de los músculos respiratorios. Estudios previos han vinculado los genotipos de factor de crecimiento insulínico 1 y 2 (IGF-1 e IGF-2) con la debilidad muscular en poblaciones sin esta enfermedad. Sin embargo, existe un vacío de conocimiento con respecto a los mecanismos biológicos subyacentes a la debilidad de los músculos respiratorios, en particular el papel de los genotipos IGF-1 e IGF-2 en esta enfermedad pulmonar. Por lo tanto, este estudio tuvo como objetivo investigar, por primera vez, la asociación de los genotipos IGF-1 e IGF-2 con la fuerza de los músculos respiratorios en individuos con enfermedad pulmonar obstructiva crónica. Además, analizamos la relación entre el estrés oxidativo, la inflamación crónica y la vitamina D con la fuerza de los músculos respiratorios. MÉTODOS: Un estudio transversal con 61 individuos con enfermedad pulmonar obstructiva crónica. Se analizó la reacción en cadena de la polimerasa de los polimorfismos genéticos IGF-1 (rs35767) e IGF-2 (rs3213221). Otras variables relacionadas con el estrés oxidativo, la inflamación y la vitamina D se dosificaron a partir de muestras de sangre periférica. Se midieron las presiones inspiratorias y espiratorias máximas. RESULTADOS: Los polimorfismos genéticos están asociados con la fuerza de los músculos respiratorios (F: 3.0 y 3.5; R2= 0.57). Genotipos específicos de IGF-1 e IGF-2 presentaron bajos valores en las presiones inspiratorias y espiratorias (p<0.05 en todos los casos). El estrés oxidativo, los biomarcadores inflamatorios y la vitamina D no se asociaron con la fuerza de los músculos respiratorios. CONCLUSIÓN: Los polimorfismos de IGF-1 e IGF-2 mostraron correlaciones más sólidas con la fuerza de los músculos respiratorios en pacientes con enfermedad pulmonar obstructiva crónica en comparación con los biomarcadores sanguíneos. Genotipos específicos de IGF-1 e IGF-2 se asociaron con una disminución de la fuerza de los músculos respiratorios en esta población.


Subject(s)
Humans , Male , Female , Middle Aged , Aged , Respiratory Muscles/physiopathology , Insulin-Like Growth Factor I/metabolism , Insulin-Like Growth Factor II/genetics , Insulin-Like Growth Factor II/metabolism , Oxidative Stress , Pulmonary Disease, Chronic Obstructive/physiopathology , Pulmonary Disease, Chronic Obstructive/genetics , Muscle Strength/physiology , Genotype , Vitamin D/blood , Cross-Sectional Studies , Muscle Weakness/physiopathology , Muscle Weakness/genetics , Inflammation/physiopathology , Inflammation/genetics
2.
Rev. Fac. Odontol. (B.Aires) ; 39(91): 67-85, 2024. ilus
Article in Spanish | LILACS | ID: biblio-1555113

ABSTRACT

Muchas investigaciones se han ocupado de evaluar la vinculación entre las afecciones bucales y otras funciones o afecciones del organismo. Algunos de esos estudios han sentado precedentes acerca de la influencia mutua que puede existir entre la fun-cionalidad de las glándulas salivales y la enfermedad periodontal, y cómo la presencia de una condición puede modificar la evolución o inducir la aparición de la otra. El objetivo del presente trabajo es hacer una revisión bibliográfica de las publicaciones cientí-ficas que evalúan los efectos de inducción recíproca que existe entre la enfermedad periodontal y la hi-posalivación. Trabajos de nuestro grupo y de otros autores demuestran que la hiposalivación reduce la capacidad del organismo para defenderse contra las bacterias patógenas, mantener un ambiente sa-ludable y facilitar la cicatrización en la cavidad bu-cal, promoviendo los procesos de inflamación y daño tisular gingivoperiodontal. A su vez, varios estudios reportan que la enfermedad periodontal induce cam-bios en las glándulas salivales y altera el volumen de secreción salival. Por su parte, el sistema endo-cannabinoide (SEC) muestra estar involucrado tanto en el proceso de secreción salival como en la infla-mación y la reabsorción ósea presentes en la enfer-medad periodontal, en tanto que la activación de los mecanismos del SEC emerge como una de las vías a través de las cuales se desarrollaría el fenómeno de inducción recíproca (AU)


Many investigations have focused on evaluating the link between oral conditions and other functions or conditions of the body. Some of these studies have set precedents about the mutual influence that may exist between the functionality of the salivary glands and periodontal disease, and how the presence of one condition can modify the evolution or induce the appearance of the other. The objective of this work is to carry out a bibliographic review of scientific publications that evaluate the reciprocal induction effects that exist between periodontal disease and hyposalivation. Studies by our group and other authors show that hyposalivation reduces the capacity of the organism to defend itself against pathogenic bacteria, maintain a healthy environment and facilitate healing in the oral cavity, promoting inflammation and gingivoperiodontal tissue damage. In turn, several studies report that periodontal disease induces changes in the salivary glands and alters the volume of salivary secretion. In turn, the endocannabinoid system (ECS) is shown to be involved in the salivary secretion process as well as in the inflammation and bone resorption present in periodontal disease, while the activation of ECS mechanisms emerges as one of the pathways through which the reciprocal induction phenomenon would develop (AU)


Subject(s)
Humans , Periodontitis/etiology , Xerostomia/etiology , Endocannabinoids , Salivary Glands/physiopathology , Oxidative Stress/physiology , Neuroinflammatory Diseases/physiopathology , Inflammation/physiopathology
3.
RFO UPF ; 28(1): 69-77, 20230808.
Article in Portuguese | LILACS, BBO | ID: biblio-1509413

ABSTRACT

Objetivo: O objetivo desta revisão de literatura é evidenciar o papel da infecção e inflamação na etiopatogenia da osteonecrose dos maxilares induzida por medicamentos (MRONJ). Revisão da literatura: A MRONJ é uma condição rara e grave que impacta negativamente a vida dos pacientes afetados. Sua etiopatogenia é multifatorial e ainda não foi totalmente compreendida. Uma das hipóteses propostas para explicá-la sugere que, além da inibição do turnover ósseo pelos medicamentos antirreabsortivos, a infecção associada à exodontia e a inflamação local desempenham papel decisivo no desencadeamento da condição. O entendimento da etiopatogenia da MRONJ permite ao cirurgião-dentista a identificação dos pacientes com risco maior para a doença, assim como o auxilia no monitoramento e escolha do manejo mais adequado. No campo da pesquisa, ele pode aprimorar estudos pré-clínicos e aprofundar a investigação de biomarcadores para diagnóstico precoce de MRONJ. Considerações finais: Conhecer a contribuição da infecção e inflamação na etiopatogênese da MRONJ é fundamental para orientar a pesquisa e a adoção de estratégias preventivas para os pacientes em risco, e de manejo e monitoramento adequado para aqueles já acometidos. (AU)


Aim: The aim of this literature review is to highlight the role of infection and inflammation in the etiopathogenesis of drug-induced osteonecrosis of the jaw (MRONJ). Literature review: MRONJ is a rare and serious condition that negatively impacts the lives of affected patients. Its etiopathogenesis is multifactorial and has not yet been fully understood. One of the hypotheses proposed to explain it suggests that, in addition to the inhibition of bone turnover by antiresorptive drugs, the infection associated with tooth extraction and local inflammation play a decisive role in triggering the condition. Understanding the etiopathogenesis of MRONJ allows the dentist to identify patients at higher risk for the disease, as well as assisting in monitoring and choosing the most appropriate management. In research, it can improve preclinical studies and deepen the investigation of biomarkers for early diagnosis of MRONJ. Conclusion: Knowing the contribution of infection and inflammation in the etiopathogenesis of MRONJ is essential to guide research and the adoption of preventive strategies for patients at risk, and adequate management and monitoring for those already affected.(AU)


Subject(s)
Humans , Bisphosphonate-Associated Osteonecrosis of the Jaw/etiology , Bisphosphonate-Associated Osteonecrosis of the Jaw/physiopathology , Inflammation/physiopathology , Bone Remodeling/drug effects , Bone Density Conservation Agents/adverse effects
4.
Rev. Asoc. Odontol. Argent ; 109(1): 41-48, ene.-abr. 2021. ilus, tab
Article in Spanish | LILACS | ID: biblio-1281207

ABSTRACT

Objetivo: En los granulomas periapicales, los plasmocitos (PL) participan activamente mediante la liberación de inmunoglobulinas. El propósito de este ensayo fue identificar y contar el número de PL en diferentes períodos de tiempo en lesiones periapicales experimentales en ratas. Materiales y métodos: Mediante la exposición al medio oral de la pulpa de los primeros molares inferiores izquierdos, se indujeron granulomas periapicales en ratas a las que previamente se les suministró anestesia. La pulpa de los primeros molares inferiores derechos no fue expuesta, y estos dientes se utilizaron como control. Los animales fueron eutanasiados a los 10, 30 y 60 días de la exposición. Los maxilares inferiores fueron removidos, y los primeros molares, junto con los tejidos circundantes, se procesaron para su estudio histológico. Se obtuvieron secciones semiseriadas, posteriormente coloreadas con verde de metilo-pironina (VMP). Cada tres secciones, las tres siguientes fueron coloreadas con hematoxilina y eosina (H-E). Los controles también fueron coloreados con H-E. Resultados: Todos los especímenes experimentales coloreados con H-E revelaron la presencia de granulomas periapicales. Luego de la exposición pulpar, el número de PL que reaccionó positivamente al VMP se incrementó de manera progresiva desde el día 10 hasta los días 30 y 60. A pesar de que a los 60 días el número de PL fue ligeramente menor que a los 30 días, no hubo diferencias estadísticamente significativas entre estos dos períodos. Los especímenes del grupo control coloreados con H-E mostraron que los tejidos periapicales se encontraban dentro de los parámetros normales en todos los períodos de observación. Conclusiones: Los resultados de este estudio revelaron que el número de plasmocitos VMP positivos se incrementa progresivamente en función del tiempo transcurrido pero se estabiliza al finalizar el experimento. También sugieren que el empleo de la coloración de VMP es un procedimiento adecuado para la identificación y la cuantificación de plasmocitos en los granulomas periapicales inducidos experimentalmente en ratas (AU)


Aim: Plasma cells (PL) release immunoglobulin in periapical lesions. The purpose of this assay was to identify and count the number of plasmocytes observed in periapical lesions in rats. Materials and methods: By exposing the pulp of the lower left first molars to the oral environment, periapical granulomas were induced in rats previously anesthetized. The pulp of right mandibular first molars was not exposed and these teeth were used as negative controls. The animals were euthanized at 10, 30 and 60 days after pup exposure. The mandibles were removed and specimens of the molar teeth along with the surrounding tissues were prepared for histology. Semi serial sections of the left first molar were stained with methyl green pyronine (MGP). Every three sections, the following three sections were stained with hematoxilyn and eosin (H-E). Negative control samples were stained with H-E. Results: All the H-E stained experimental samples revealed the presence of periapical granulomas. After pulp exposure, the number of PL increased from day 10 to 30 and 60. In the 60-day samples the number of PL was slightly less than that of the 30-day samples, with no statistically significant difference. The H-E stained control samples showed normal periapical tissues in all observation periods. Conclusions: The results of this study revealed that the number of VMP positive PL, increased progressively with time but it was stabilized at the end of the experiment. In addition, the results suggest that the use of VMP stain is a suitable procedure for the identification and counting of PL in experimentally induced periapical granulomas in rats (AU)


Subject(s)
Animals , Rats , Periapical Granuloma/immunology , Plasma Cells/immunology , Inflammation/physiopathology , Periapical Tissue , Immunoglobulins , Photomicrography , Histological Techniques , Radiography, Dental, Digital
5.
Rev. bras. cir. cardiovasc ; Rev. bras. cir. cardiovasc;35(5): 757-763, Sept.-Oct. 2020. tab, graf
Article in English | LILACS, SES-SP | ID: biblio-1137320

ABSTRACT

Abstract It has been reported that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection induces endothelial inflammation, therefore facilitating the progression of endothelial and vascular dysfunction in coronavirus disease 2019 (COVID-19) patients. Coronary artery bypass grafting (CABG) involves mainly the use of the saphenous vein (SV) and internal mammary artery as graft material in the stenosed coronary arteries. Unfortunately, graft patency of the SV is low due to endothelial dysfunction and inflammation. We propose that SARS-CoV-2 might cause vascular inflammation, endothelial dysfunction, and thrombosis in coronary artery bypass graft vessels by binding angiotensin-converting enzyme 2 receptor. Therefore, in this Special Article, we consider the potential influence of COVID-19 on the patency rates of coronary artery bypass graft vessels, mainly with reference to the SV. Moreover, we discuss the technique of SV graft harvesting and the therapeutic potential of focusing on endothelial dysfunction, vascular inflammation, and thrombosis for protecting coronary artery bypass grafts in COVID-19 infected CABG patients.


Subject(s)
Humans , Vascular Patency , Coronary Artery Bypass , Coronavirus Infections/complications , Graft Occlusion, Vascular/virology , Saphenous Vein/surgery , Thrombosis/physiopathology , Endothelium, Vascular/physiopathology , Treatment Outcome , Betacoronavirus , Inflammation/physiopathology
6.
Arq. bras. cardiol ; Arq. bras. cardiol;114(1): 100-105, Jan. 2020. tab, graf
Article in English | LILACS | ID: biblio-1055084

ABSTRACT

Abstract Background: The emergence of coronary heart disease is increased with menopause, physical inactivity and with dyslipidemia. Physical training is known to promote the improvement of cardiovascular functions. Objective: To investigate the effects of aerobic physical training on the left ventricle in ovariectomized LDL knockout mice. Methods: Thirty animals were divided into 6 groups (n = 5): Sedentary non-ovariectomized control; Sedentary ovariectomized control; Trained ovariectomized control; Sedentary non-ovariectomized LDL-knockout, sedentary ovariectomized LDL-knockout and trained ovariectomized LDL-knockout. We analyzed the average parameters of apparent density of collagen fibers types I and III, and metalloproteinase type 2 and type 9, were considered significant p < 0.05. Results: The results showed that the proposed exercise protocol altered the volume of type I collagen fibers, altered collagen remodeling parameters (MMP-2), and also reduced the 8-hydroxy-2'-deoxyguanosine (8OHdG) oxidative stress parameter. Conclusion: Moderate intensity aerobic training acts on collagen fiber volume, on collagen remodeling with the reduction of oxidative stress in the left ventricles of ovariectomized LDL-knockout mice.


Resumo Fundamento: O surgimento da doença cardíaca coronariana aumenta com a menopausa, inatividade física e dislipidemia. Sabe-se que o treinamento físico promove a melhora das funções cardiovasculares Objectivo: Investigar os efeitos do treinamento físico aeróbico sobre o ventrículo esquerdo em camundongos LDL knockout ovariectomizadas. Métodos: Trinta animais foram divididos em 6 grupos (n = 5): controle sedentário não ovariectomizado, controle sedentário ovariectomizado, controle treinado ovariectomizado, sedentário LDL-knockout não ovariectomizado, sedentário LDL-knockout ovariectomizado e treinado LDL-knockout ovariectomizado. Analisamos os parâmetros médios da densidade de volume de fibras colágenas tipo I e III, e metaloproteinases 2 e 9. Valores de p < 0,05 foram considerados significativos. Resultados: Os resultados mostram que o protocolo de exercício proposto alterou o volume de fibras colágenas do tipo I e os parâmetros de remodelamento do colágeno (MMP-2), e ainda reduziu o parâmetro de estresse oxidativo do 8-hidroxi-2'-deoxiganosina (8-OhdG). Conclusão: O treinamento aeróbico de intensidade moderada age sobre o volume das fibras colágenas e sobre o remodelamento de colágeno, com redução do estresse oxidativo em ventrículos esquerdos de camundongos ovariectomizados LDLr Knockout.


Subject(s)
Animals , Female , Rats , Matrix Metalloproteinase 2/metabolism , Matrix Metalloproteinase 9/metabolism , Collagen Type I/metabolism , Collagen Type III/metabolism , Inflammation/physiopathology , Myocardium/metabolism , Physical Conditioning, Animal/physiology , Immunohistochemistry , Ovariectomy , Mice, Knockout , Oxidative Stress/physiology , Models, Animal
7.
Braz. J. Pharm. Sci. (Online) ; 56: e18567, 2020. tab, graf
Article in English | LILACS | ID: biblio-1249167

ABSTRACT

Microbial translocation is associated with the increased risk of cardiovascular disease in HIV-infected individuals. There is scarce information regarding the possible associations between the biomarkers of microbial translocation, inflammation and cardiovascular risk that can be evaluated in clinical laboratories using plasma or serum samples. This systematic review was conducted according to the PRISMA protocol in order to verify the most used soluble biomarkers of microbial translocation, inflammation and cardiovascular risk, as well as possible associations between them, in HIV-infected individuals. A search was performed using the Medline, Scopus and Web of Science databases to identify existing studies regarding the relationship between microbial translocation biomarkers, inflammation and cardiovascular risk in HIV-infected patients. Eleven articles that presented soluble biomarkers of microbial translocation (LPS, rDNA, sCD14, LBP and EndoCAb) were selected. The most frequently evaluated soluble biomarker was sCD14, followed by LPS; the latter were associated with some lipid profile parameters. This systematic review considered soluble blood biomarkers that can be utilized in laboratory diagnosis. The aim was to identify the interconnection between microbial translocation, inflammation and cardiovascular risk. Despite the fact that a large number of inflammation and cardiovascular risk biomarkers have been previously reported, it was noted that important markers involved in the pathophysiology of cardiovascular diseases need to be included in future research.


Subject(s)
Patients/classification , Biomarkers/analysis , Cardiovascular Diseases/physiopathology , HIV/pathogenicity , Systematic Review , Heart Disease Risk Factors , Inflammation/physiopathology , Blood , Risk , Lipopolysaccharide Receptors , Clinical Laboratory Techniques/instrumentation
8.
Einstein (São Paulo, Online) ; 18: eAO4784, 2020. tab, graf
Article in English | LILACS | ID: biblio-1039736

ABSTRACT

ABSTRACT Objective To evaluate the effect of three types of muscular resistance training on adiposity, inflammation levels and insulin activity in Swiss mice with fat-rich diet-induced obesity. Methods Lean and obese male Swiss mice were selected and allocated to one of eight groups comprising eight mice each, as follows: standard diet + no training; standard diet + muscular resistance training; standard diet + hypertrophy training; standard diet + strength training; high-fat diet + no training; high-fat diet + muscular resistance training; high-fat diet + hypertrophy training; high-fat diet + strength training. The training protocol consisted of stair climbing for a 10-week period. Blood samples were collected for lactate analysis, glucose level measurement and insulin tolerance test. After euthanasia, adipose tissues were removed and weighed for adiposity index determination. Fragments of epididymal adipose tissue were then embedded for histological analysis or homogenized for tumor necrosis factor alpha level determination using the ELISA method. Results Ausency of differences in total training volume and blood lactate levels overall emphasize the similarity between the different resistance training protocols. Body weight loss, reduced adipocyte area and lower adiposity index were observed in trained obese mice, regardless of training modality. Different training protocols also improved insulin sensitivity and reduced inflammation levels. Conclusion Resistance training protocols were equally effective in reducing body fat, inflammation levels and insulin resistance in obese mice.


RESUMO Objetivo Avaliar os efeitos de três tipos de treinamentos de resistência na adiposidade, na inflamação e na ação da insulina em camundongos Swiss obesos por dieta hiperlipídica. Métodos Camundongos Swiss machos magros e obesos foram selecionados e posteriormente separados em oito grupos com oito animais em cada: dieta padrão + não treinado; dieta padrão + treinamento de resistência muscular; dieta padrão + treinamento de hipertrofia; dieta padrão + treinamento de força; dieta hiperlipídica + não treinado; dieta hiperlipídica + treinamento de resistência muscular; dieta hiperlipídica + treinamento de hipertrofia; e dieta hiperlipídica + treinamento de força. O protocolo de treinamento consistiu em escaladas, por um período de 10 semanas. Amostras de sangue foram coletadas para análises de lactato, glicemia e teste de tolerância à insulina. Após eutanásia, os tecidos adiposos foram retirados e pesados para determinar o índice de adiposidade. Em seguida, parte do tecido adiposo epididimal foi emblocado para análises histológicas, e outra parte foi homogeneizada para análises de fator de necrose tumoral alfa por ELISA. Resultados O volume total de treinamento e a concentração sanguínea de lactato não diferiram entre os três treinos resistidos, sugerindo similaridade entre eles. Nos animais obesos, as três modalidades de treinamento reduziram o peso corporal, a área adipocitária e o índice de adiposidade. Os três tipos de treinamentos ainda melhoraram a tolerância à insulina e reduziram a inflamação. Conclusão Os protocolos de treinamento resistido foram igualmente efetivos em reduzir a adiposidade, a inflamação e a resistência à ação da insulina em camundongos obesos.


Subject(s)
Animals , Male , Mice , Physical Conditioning, Animal/physiology , Insulin Resistance/physiology , Adiposity/physiology , Muscle Stretching Exercises/methods , Hypertrophy/physiopathology , Inflammation/physiopathology , Obesity/physiopathology , Time Factors , Blood Glucose/analysis , Body Weight/physiology , Enzyme-Linked Immunosorbent Assay , Reproducibility of Results , Tumor Necrosis Factor-alpha/analysis , Adipose Tissue, White/physiopathology , Resistance Training/methods , Diet, High-Fat , Mice , Mice, Obese
9.
Arch. Clin. Psychiatry (Impr.) ; Arch. Clin. Psychiatry (Impr.);46(5): 137-140, Sept.-Oct. 2019. tab, graf
Article in English | LILACS | ID: biblio-1054909

ABSTRACT

Abstract Background Inflammation is involved in the pathophysiology of depression, and circulating inflammatory cytokines have been associated with depressive symptoms. However, measuring circulating cytokines have inherent methodological limitations. In vitro lipopolysaccharide (LPS)-stimulated intracellular cytokines (ICCs) overcome these limitations. Furthermore, because psychosocial and physiological stressors activate inflammatory responses and LPS-stimulated ICCs reflect the inflammatory responsivity of monocytes to such stressors, ICCs may reflect individual stress responsivity. Methods This cross-sectional study examined whether LPS-stimulated expression of ICCs in peripheral blood mononuclear cells (PBMCs) is a sensitive inflammation measure correlated with depressive symptoms in 180 community-dwelling older adults. We tested correlations of not only intracellular but also circulating inflammatory markers with depressive symptoms assessed using the 10-item Center for Epidemiological Studies Depression Scale (CES-D). Intracellular markers included expression of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and both in PBMCs. Circulating markers included IL-6, TNF-α, and C-reactive protein (CRP) in plasma. Results None of the correlations were statistically significant. However, in contrast to circulating markers, the correlations of ICCs were consistently in the expected direction, i.e., higher ICC expression correlating with higher depression severity. Discussion Despite the non-significant findings, further research is required for the evaluation of LPS-stimulated ICC expression as biomarkers of depressive symptoms.


Subject(s)
Humans , Male , Female , Middle Aged , Aged , Aged, 80 and over , Lipopolysaccharides , Cytokines/blood , Depression/physiopathology , Inflammation/physiopathology , Psychiatric Status Rating Scales , In Vitro Techniques , C-Reactive Protein , Monocytes/metabolism , Biomarkers/blood , Cross-Sectional Studies , Interleukin-6/blood , Tumor Necrosis Factor-alpha/blood , Depression/blood , Inflammation/blood
10.
J. pediatr. (Rio J.) ; J. pediatr. (Rio J.);95(5): 575-583, Sept.-Oct. 2019. tab
Article in English | LILACS | ID: biblio-1040361

ABSTRACT

Abstract Objective: Evaluate the association between inflammatory process, adiposity, and vitamins A, D, and E in adolescents, according to gender. Methods: Cross-sectional study with adolescents aged 12-19 years old of both genders attending public schools in Recife. A questionnaire was used to collect data on socioeconomic level, lifestyle, and food intake of adolescents. Then, an anthropometric evaluation and a blood sampling were performed to analyze serum concentrations of α-1-acid glycoprotein, retinol, β-carotene, α-tocopherol, and 25-hydroxy-vitamin D. Results: The levels of α-1-acid glycoprotein were higher for abdominal obesity in both genders. Male adolescents with insufficient serum α-tocopherol levels had low levels of α-1-acid glycoprotein (p = 0.03) and an increased risk of 25-hydroxy-vitamin D and β-carotene deficiency in relation to total and abdominal fat; female adolescents had an increased risk of insufficient β-carotene with abdominal obesity (PR: 1.33; 95% CI: 1.2-1.5). Conclusion: Abdominal adiposity implies a higher risk of inflammation and causes different changes to the levels of fat-soluble vitamins according to gender.


Resumo: Objetivo: Avaliar a associação entre processo inflamatório, adiposidade e as vitaminas A, D e E em adolescentes, segundo o sexo. Métodos: Estudo transversal com adolescentes de 12 a 19 anos de ambos os sexos de escolas públicas de Recife. Foi utilizado um questionário para coleta de dados socioeconômicos, de estilo de vida e de consumo alimentar dos adolescentes. Em seguida, realizou-se a avalição antropométrica e coleta de sangue para análise das concentrações séricas de α-1-glicoproteína ácida, retinol, β-caroteno, α-tocoferol e 25-hidroxivitamina D. Resultados: Os níveis de α-1-glicoproteína ácida foram maiores na obesidade abdominal de ambos os sexos. Os meninos com níveis séricos insuficientes de α-tocoferol expressaram níveis reduzidos de α-1-glicoproteína ácida (p = 0,03) e apresentaram um maior risco de deficiência de 25-hidroxivitamina D e β-caroteno na adiposidade total e abdominal, enquanto as meninas mostraram maior risco de insuficiência de β-caroteno com a obesidade abdominal (RP 1,33; IC 95% 1,2-1,5). Conclusão: A adiposidade abdominal reflete maior risco de inflamação e causa alterações distintas nas concentrações das vitaminas lipossolúveis, de acordo com o sexo.


Subject(s)
Humans , Female , Child , Adolescent , Vitamins/metabolism , Adiposity/physiology , Inflammation/metabolism , Obesity/metabolism , Reference Values , Vitamin D/analogs & derivatives , Orosomucoid/analysis , Carotenoids/blood , Anthropometry , Nutritional Status , Cross-Sectional Studies , Inflammation/etiology , Inflammation/physiopathology , Obesity/complications , Obesity/physiopathology
11.
Rev. chil. enferm. respir ; Rev. chil. enferm. respir;35(2): 124-132, jun. 2019. graf
Article in Spanish | LILACS | ID: biblio-1042621

ABSTRACT

La sarcopenia es una enfermedad caracterizada por la pérdida de masa muscular, fuerza muscular y rendimiento físico, siendo la principal causa de fragilidad en los adultos mayores. La sarcopenia es altamente prevalente en individuos con enfermedad pulmonar obstructiva crónica (EPOC) que conduce a un mal pronóstico y una mayor mortalidad en esta población. La presencia de sarcopenia en la EPOC es probablemente el resultado de la interacción entre factores externos e internos como la inflamación sistémica, el estrés oxidativo y los polimorfismos genéticos, frecuentemente observados en individuos con esta enfermedad respiratoria. Esta revisión resume el conocimiento sobre los mecanismos patogénicos asociados con la sarcopenia en la EPOC.


Sarcopenia is a disease characterized by loss of skeletal muscle, muscle strength and physical performance, being the major cause of frailty in the elderly. The sarcopenia is highly prevalent in individuals with Chronic obstructive pulmonary disease (COPD) leading to a poor prognosis and higher mortality in this population. The presence of sarcopenia in COPD is likely the result by the interaction between external and internal factors as systemic inflammation, oxidative stress and genetic polymorphisms, frequently observed in individuals with this respiratory disease. This review summarizes the current knowledge about the pathogenic mechanisms linking COPD with sarcopenia.


Subject(s)
Humans , Pulmonary Disease, Chronic Obstructive/physiopathology , Sarcopenia/physiopathology , Polymorphism, Genetic , Aging , Risk Factors , Oxidative Stress/physiology , Sarcopenia/genetics , Inflammation/physiopathology
12.
Fisioter. Pesqui. (Online) ; 26(2): 164-169, abr.-jun. 2019. graf
Article in English | LILACS | ID: biblio-1012148

ABSTRACT

ABSTRACT Nicotine delays the healing process and increases the levels of myeloperoxidase (MPO), an enzyme that plays a key role in the production of reactive oxygen species during the inflammatory process. Laser Photobiomodulation (PBM) is one of the most used electrophysical agents in the treatment of the calcaneal tendon, however, its effects on MPO activity need to be further elucidated. This study aimed to evaluate the effects of laser PBM on MPO activity after inflicting an injury to the calcaneal tendon of rats exposed to cigarette smoke. Thirty-four male Wistar rats with 90 days of age were used. After 14 days of exposure to cigarette smoke, the animals were divided into three experimental groups: control group (CG, n=12), not submitted to injury or treatment; sham group (ShG, n=10), submitted to partial calcaneal tendon injury and laser PBM simulation; and laser PBM group (PBMG, n=12), submitted to partial calcaneal tendon lesion and treated with laser PBM within the first minute after injury. PBM decreased MPO activity levels in PBMG compared to ShG (CG: 1.38±0.69pg/ml; ShG: 3.78±1.09pg/ml; PBMG: 2.58±0.93pg/ml; p<0.005). In conclusion, applying laser PBM immediately after inflicting damage to the calcaneal tendon attenuates acute inflammatory activity in rats exposed to cigarette smoke.


RESUMO A nicotina retarda o processo de cicatrização e eleva os níveis da enzima mieloperoxidase (MPO), a qual possui um papel fundamental na produção de espécies reativas de oxigênio durante o processo inflamatório. A fotobiomodulação laser (FBM) é um dos agentes eletrofísicos mais utilizados no tratamento do tendão calcâneo, no entanto, os seus efeitos sobre a atividade da MPO carecem de maior elucidação. Este estudo objetivou avaliar os efeitos da FBM sobre a atividade da MPO, após lesão do tendão calcâneo em ratos expostos à fumaça de cigarro. Foram utilizados 34 ratos Wistar, machos, com 90 dias de vida. Após 14 dias de exposição à fumaça de cigarro, os animais foram divididos em três grupos experimentais: grupo controle (GC, n=12), não submetido à lesão ou tratamento; grupo sham (GSh, n=10), submetido à lesão parcial do tendão calcâneo e a simulação da FBM laser; grupo FBM laser (GFBM, n=12), submetido à lesão parcial do tendão calcâneo e tratados com FBM laser, no primeiro minuto após a lesão. A FBM diminuiu os níveis de atividade da MPO no GFBM em comparação ao GSh (GC: 1,38±0,69 pg/ml; GSh: 3,78±1,09pg/ml; GFBM: 2,58±0,93pg/ml; p<0,005). Conclui-se que a FBM laser aplicada imediatamente após lesão do tendão calcâneo, atenua a atividade inflamatória aguda em ratos expostos à fumaça de cigarro.


RESUMEN La nicotina retarda el proceso de cicatrización y eleva los niveles de la enzima mieloperoxidasa (MPO), que tiene un papel fundamental en la producción de especies reactivas de oxígeno durante el proceso inflamatorio. La fotobiomodulación con láser (FBM) es uno de los agentes electrofísicos más utilizados en el tratamiento del tendón calcáneo, sin embargo sus efectos sobre la actividad de la MPO carecen de mayor elucidación. Este estudio objetivó evaluar los efectos de la FBM sobre la actividad de la MPO después de lesión del tendón calcáneo en ratones expuestos al humo de cigarrillo. Se utilizaron 34 ratones Wistar, machos, con 90 días de vida. Después de 14 días de exposición al humo de cigarrillo, los animales fueron divididos en tres grupos experimentales: grupo de control (GC, n=12), no sometido a la lesión o tratamiento; grupo sham (GSh, n=10), sometido a la lesión parcial del tendón calcáneo y a la simulación de la FBM láser; y el grupo FBM láser (GFBM, n=12), sometido a la lesión parcial del tendón calcáneo y tratado con FBM láser, en el primer minuto después de la lesión. La FBM disminuyó los niveles de actividad de MPO en el GFBM en comparación con el GSh (GC: 1,38±0,69 pg/ml; GSh: 3,78±1,09pg/ml; GFBM: 2,58±0,93pg/ml, p<0,005). Se concluye que la FBM láser aplicada inmediatamente después de la lesión del tendón calcáneo atenúa la actividad inflamatoria aguda en ratones expuestos al humo de cigarrillo.


Subject(s)
Animals , Achilles Tendon/physiopathology , Tobacco Smoke Pollution/adverse effects , Low-Level Light Therapy , Tendinopathy/therapy , Wound Healing/physiology , Rats, Wistar , Models, Animal , Inflammation/physiopathology , Nicotine/adverse effects
13.
Arq. bras. cardiol ; Arq. bras. cardiol;112(5): 577-587, May 2019. tab, graf
Article in English | LILACS | ID: biblio-1011188

ABSTRACT

Abstract Chronic hyperglycemia is the key point of macro- and microvascular complications associated with diabetes mellitus. Excess glucose is responsible for inducing redox imbalance and both systemic and intrarenal inflammation, playing a critical role in the pathogenesis of diabetic kidney disease, which is currently the leading cause of dialysis in the world. The pathogenesis of the disease is complex, multifactorial and not fully elucidated; many factors and mechanisms are involved in the development, progression and clinical outcomes of the disease. Despite the disparate mechanisms involved in renal damage related to diabetes mellitus, the metabolic mechanisms involving oxidative/inflammatory pathways are widely accepted. The is clear evidence that a chronic hyperglycemic state triggers oxidative stress and inflammation mediated by altered metabolic pathways in a self-perpetuating cycle, promoting progression of cell injury and of end-stage renal disease. The present study presents an update on metabolic pathways that involve redox imbalance and inflammation induced by chronic exposure to hyperglycemia in the pathogenesis of diabetic kidney disease.


Resumo A hiperglicemia crônica é o ponto-chave das complicações macro e microvasculares associadas ao diabetes mellitus. O excesso de glicose é responsável por induzir desequilíbrio redox e inflamação sistêmica e intra-renal, desempenhando um papel crítico na patogênese da doença renal do diabetes, configurada atualmente como a principal causa de doença renal dialítica em todo o mundo. A patogênese da doença é complexa, multifatorial e, não totalmente elucidada, estando vários fatores e mecanismos associados ao seu desenvolvimento, progressão e desfechos clínicos. Apesar dos mecanismos díspares envolvidos nos danos renais durante o diabetes, os caminhos metabólicos pela via oxidativa/inflamatória são amplamente aceitos e discutidos. As evidências acentuam que o estado hiperglicêmico crônico desencadeia o estresse oxidativo e a inflamação mediada por diversas vias metabólicas alteradas em um ciclo-vicioso de autoperpetuação, promovendo aumento da injúria celular e progressão para a doença renal dialítica. O presente artigo traz, portanto, uma atualização sobre os caminhos metabólicos que envolvem o desequilíbrio redox e a inflamação induzidos pela exposição crônica à hiperglicemia na patogênese da doença renal do diabetes.


Subject(s)
Humans , Oxidation-Reduction , Oxidative Stress/physiology , Diabetic Nephropathies/etiology , Hyperglycemia/complications , Inflammation/etiology , Chronic Disease , Disease Progression , Diabetic Nephropathies/physiopathology , Hyperglycemia/physiopathology , Inflammation/physiopathology
14.
Arq. bras. cardiol ; Arq. bras. cardiol;112(5): 545-552, May 2019. tab, graf
Article in English | LILACS | ID: biblio-1011190

ABSTRACT

Abstract Background: Obesity can be characterized by low-grade chronic inflammation and is associated with an excesso production of reactive oxygen species, factors that contribute to coronary heart disease and other cardiomyopathies. Objective: To verify the effects of resistance exercise training on oxidative stress and inflammatory parameters on mice with obesity induced by a high-fat diet (HFD). Methods: 24 Swiss mice were divided into 4 groups: standard diet (SD), SD + resistance exercise (SD + RE), diet-induced obesity (DIO), DIO + RE. The animals were fed SD or HFD for 26 weeks and performed resistance exercises in the last 8 weeks of the study. The insulin tolerance test (ITT) and body weight monitoring were performed to assess the clinical parameters. Oxidative stress and inflammation parameters were evaluated in the cardiac tissue. Data were expressed by mean and standard deviation (p < 0.05). Results: The DIO group had a significant increase in reactive oxygen species levels and lipid peroxidation with reduction after exercise. Superoxide dismutase and the glutathione system showed no significant changes in DIO animals, with an increase in SD + RE. Only catalase activity decreased with both diet and exercise influence. There was an increase in tumor necrosis factor-alpha (TNF-α) in the DIO group, characterizing a possible inflammatory condition, with a decrease when exposed to resistance training (DIO+RE). Conclusion: The DIO resulted in a redox imbalance in cardiac tissue, but the RE was able to modulate these parameters, as well as to control the increase in TNF-α levels.


Resumo Fundamento: A obesidade pode ser caracterizada por uma inflamação crônica de baixo grau e está associada à produção excessiva de espécies reativas de oxigênio, fatores que contribuem para doenças coronarianas e outras cardiomiopatias. Objetivo: Verificar os efeitos do treinamento resistido sobre os parâmetros de estresse oxidativo e parâmetro inflamatório em camundongos com obesidade induzida por dieta hiperlipídica (DIO). Métodos: 24 camundongos Swiss foram divididos em 4 grupos: dieta padrão (DP), DP + exercício resistido (DP+ER), obesidade induzida por DIO, DIO + ER. Os animais foram alimentados por 26 semanas com DP ou hiperlipídica realizando treinamento resistido nas 8 semanas finais do estudo. Para avaliar parâmetros clínicos foi realizado o teste de tolerância à insulina (TTI) e monitoramento do peso corporal. No tecido cardíaco foram avaliados parâmetros de estresse oxidativo e inflamação. Dados expressos por média e desvio padrão (p < 0,05). Resultados: O grupo DIO teve um aumento significativo nos níveis espécies reativas e peroxidação lipídica com redução após o exercício. A superóxido dismutase e o sistema glutationa não demonstraram alterações importantes nos animais DIO, com elevação perante DP+ER. Somente a atividade da catalase reduziu tanto com influência da dieta como do exercício. Ocorreu um aumento do fator de necrose tumoral-alfa (TNF-α) no grupo DIO, caracterizando um possível quadro inflamatório, com redução quando expostos ao treino resistido (DIO+ER). Conclusão: A DIO ocasionou um desequilíbrio redox no tecido cardíaco, porém o ER foi capaz de modular estes parâmetros, bem como controlar o aumento do TNF-α.


Subject(s)
Animals , Male , Rats , Lipid Peroxidation/physiology , Tumor Necrosis Factor-alpha/analysis , Oxidative Stress/physiology , Resistance Training , Diet, High-Fat/adverse effects , Myocardium/chemistry , Physical Conditioning, Animal , Time Factors , Insulin Resistance , Inflammation/physiopathology
15.
Int. j. cardiovasc. sci. (Impr.) ; 32(2): 118-124, mar.-abr. 2019. tab
Article in English | LILACS | ID: biblio-987759

ABSTRACT

Background: Inflammation is a major component of the response to tissue injury caused by myocardial infarction. High-sensitivity C-reactive protein (hs-CRP) levels might be a simple marker of the severity of this inflammatory response, providing prognostic information. Objective: To associate hs-CRP level on admission and other clinical characteristics with in-hospital mortality of patients with acute ST-segment elevation myocardial infarction (STEMI). Methods: A retrospective cohort study of patients admitted with STEMI was carried out. Patients were analyzed regarding clinical characteristics, reperfusion therapy, hs-CRP on admission and outcomes. Continuous variables were analyzed by non-parametric Mann-Whitney U test and categorical variables by chi-square test. A p value of < 0.05 was considered statistically significant. Results: Of the 118 patients analyzed, 20 died during hospitalization. Higher levels of hs-CRP (p = 0.001) and older ages (p = 0.003) were observed among those patients who died. Logistic regression showed that a one unit increase in hs-CRP increased the risk of death by 15% (p = 0.0017), after adjustment for established risk factors. Similarly, each one-year increase in age increases the risk of death by 6.6% (p = 0.003). Conclusion: Our results demonstrate a strong association between hs-CRP obtained on admission and in-hospital mortality after STEMI. It suggests that hs-CRP can be a marker of inflammatory response to myocardial ischemia, providing prognostic information regarding the risk of death


Subject(s)
Humans , Male , Female , Middle Aged , C-Reactive Protein , Biomarkers , Myocardial Infarction/mortality , Prognosis , Cardiovascular Diseases/mortality , Body Mass Index , Retrospective Studies , Risk Factors , Hospital Mortality , Diabetes Mellitus , Inflammation/physiopathology
16.
Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;52(2): e7773, 2019. tab, graf
Article in English | LILACS | ID: biblio-984030

ABSTRACT

The aim of this study was to evaluate the therapeutic effects of ultrasound (US)-mediated phonophoresis alone or in association with diclofenac diethylammonium (DCF) administered topically in animal models of inflammation. A pre-clinical, prospective, and randomized experimental study of quantitative and qualitative nature was carried out. Phonophoresis was performed using a therapeutic ultrasound apparatus in two distinct models of acute inflammation. Edema was induced by an intraplantar injection of carrageenan and measured by plethysmography. The Hargreaves test was used to evaluate the antinociceptive activity and investigate the action of phonophoresis on tumor necrosis factor (TNF)-α production. A histological analysis with hematoxylin-eosin was used to evaluate tissue repair, and the expression of COX-2 was determined by immunohistochemical analysis. At the peak of inflammatory activity (3 h), treatment with US, US+DCF, and DCF significantly reduced edema formation compared to the control group. Treatment with US+DCF was more effective than treatment with US alone at both analyzed times. In the analysis of the antinociceptive activity, the treatments significantly increased the latency time in response to the thermal stimulus. Histopathological analysis revealed a reduction of the inflammatory infiltrates and immunohistochemistry demonstrated that the association was effective in reducing COX-2 expression compared to the control group. The association of DCF with US produced anti-inflammatory and antinociceptive effects in rat models of inflammation, which may be associated with inhibition of COX-2 and TNF-α production.


Subject(s)
Animals , Male , Rats , Phonophoresis , Anti-Inflammatory Agents, Non-Steroidal/administration & dosage , Diclofenac/administration & dosage , Analgesics/administration & dosage , Inflammation/drug therapy , Anti-Inflammatory Agents/administration & dosage , Ultrasonic Therapy/methods , Random Allocation , Prospective Studies , Administration, Topical , Tumor Necrosis Factor-alpha , Rats, Wistar , Disease Models, Animal , Inflammation/physiopathology , Inflammation/pathology
17.
Int. arch. otorhinolaryngol. (Impr.) ; 23(2): 241-249, 2019. ilus, tab
Article in English | LILACS | ID: biblio-1015650

ABSTRACT

Introduction: The importance of our study lies in the fact that we have demonstrated the occurrence ofmechanical dysfunction within polypoid tissues, which promotes the development of polyps in the nasal cavity. Objective: To change the paradigm of nasal polyposis (NP). In this new conception, the chronic nasal inflammatory process that occurs in response to allergies, to pollution, to changes in the epithelial barrier, or to other factors is merely the trigger of the development of the disease in individuals with a genetic predisposition to an abnormal tissue remodeling process, which leads to a derangement of the mechanical properties of the nasal mucosa and, consequently, allows it to grow unchecked. Data: Synthesis We propose a fundamentally new approach to intervening in the pathological process of NP, addressing biomechanical properties, fluid dynamics, and the concept of surface tension. Conclusion: The incorporation of biomechanical knowledge into our understanding of NP provides a new perspective to help elucidate the physiology and the pathology of nasal polyps, and new avenues for the treatment and cure of NP (AU)


Subject(s)
Humans , Nasal Polyps/physiopathology , Nasal Polyps/pathology , Inflammation/physiopathology , Sinusitis/physiopathology , Biomechanical Phenomena , Brazil , Flow Mechanics , Chronic Disease , Edema/physiopathology , Extracellular Matrix/pathology , Hydrostatic Pressure , Nasal Mucosa/physiopathology , Nasal Mucosa/pathology
18.
Braz. oral res. (Online) ; 33: e060, 2019. tab, graf
Article in English | LILACS | ID: biblio-1011656

ABSTRACT

Abstract This study evaluated the effect of hypertension on tissue response and biomineralization capacity of white Mineral Trioxide Aggregate (MTA), High-plasticity MTA (MTA HP), and Biodentine® (BDT) in rats. Polyethylene tubes filled with MTA, MTA HP, BDT, and the control group (empty tubes) were placed into the dorsal subcutaneous tissue of 32 male rats (16 normotensive (NT) and 16 hypertensive rats - 8 per group). After 7 and 30 days, the polyethylene tubes surrounded by connective tissue were removed, fixed, and embedded in histological resin. The mean number of inflammatory cells was estimated in HE-stained sections, biomineralization was quantified as area (µm2) by Kossa (VK) staining, and examination by polarized light (LP) microscopy was performed. The differences amongst the groups were analyzed statistically by the Mann-Whitney or Student's t test, according to Shapiro-Wilk test of normality (p < 0.05). The inflammatory responses to all materials were greater in hypertensive rats than in NT rats (p < 0.05). Positive VK staining in MTA and BDT were more pronounced in NT rats at 7 and 30 days (p < 0.05). Birefringent structures in LP for MTA, MTA HP, and BDT were more pronounced in NT rats at 7 days (p<0.05). In rats, hypertension was able to increase inflammatory infiltrate and decrease biomineralization of the tested materials.


Subject(s)
Oxides/pharmacology , Biocompatible Materials/pharmacology , Silicates/pharmacology , Calcium Compounds/pharmacology , Aluminum Compounds/pharmacology , Subcutaneous Tissue/drug effects , Subcutaneous Tissue/physiopathology , Biomineralization/physiology , Hypertension/physiopathology , Time Factors , Materials Testing , Reproducibility of Results , Rats, Wistar , Subcutaneous Tissue/pathology , Drug Combinations , Hypertension/complications , Inflammation/physiopathology , Inflammation/pathology , Microscopy, Polarization
19.
In. Boggia de Izaguirre, José Gabriel; Hurtado Bredda, Francisco Javier; López Gómez, Alejandra; Malacrida Rodríguez, Leonel Sebastián; Angulo Nin, Martín; Seija Alves, Mariana; Luzardo Domenichelli, Leonella; Gadola Bergara, Liliana; Grignola Rial, Juan Carlos. Fisiopatología: mecanismos de las disfunciones orgánicas. Montevideo, BiblioMédica, 2 ed; c2019. p.55-66, ilus, tab.
Monography in Spanish | LILACS, UY-BNMED, BNUY | ID: biblio-1435045
20.
Rev. bras. neurol ; 54(3): 22-27, jul.-ago. 2018. ilus, tab
Article in Portuguese | LILACS | ID: biblio-948073

ABSTRACT

A esclerose lateral amiotrófica (ELA) esporádica é uma doença neurodegenerativa que acomete o neurônio motor. Sua etiologia ainda não foi totalmente esclarecida e é considerada multifatorial. O objetivo desse trabalho é fazer uma revisão narrativa sobre os mecanismos fisiopatológicos da ELA esporádica, com foco no papel da neuroinflamação, além de descrever estudos envolvendo a pesquisa de biomarcadores de diagnóstico e prognóstico. O processo de neuroinflamação na ELA é considerado secundário às alterações que levam à morte neuronal, podendo influenciar na taxa de progressão da doença. Existem diversos estudos sobre o perfil dos fatores inflamatórios na ELA, por vezes com resultados contraditórios, reforçando a dificuldade de análise desses fatores num organismo dinâmico. Ainda assim, no contexto da ELA, o estudo de possíveis biomarcadores diagnósticos e/ou prognósticos é válido e de grande interesse, pois permitiria um avanço nos ensaios clínicos que buscam novos tratamentos, bem como na condução e planejamento de cada caso.


Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that affects the motor neuron. Its etiology has not been fully clarified and is considered multifactorial. The aim of this sudy is to perform a narrative review on the pathophysiological mechanisms of sporadic ALS, focusing on the role of neuroinflammation. It will also discuss studies investigating diagnostic and prognostic biomarkers. Neuroinflammation in ALS is considered to be a secondary event, triggered by neuronal death, and it may influence disease progression. There are several studies on inflammatory factors in ALS, some with contradictory findings, reinforcing the difficulty of assessing these factors in a dynamic organism. Even so, in ALS context, the study of possible diagnostic and/or prognostic biomarkers is valid and of great interest. This may allow the advance of clinical trials that investigate new treatments, as well as the management of individual cases.


Subject(s)
Humans , Amyotrophic Lateral Sclerosis/diagnosis , Amyotrophic Lateral Sclerosis/physiopathology , Inflammation/physiopathology , Biomarkers/blood , Longitudinal Studies , Inflammation Mediators , Disease Progression , Systematic Reviews as Topic
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