Aerobic exercise training attenuates detrimental effects of cigarette smoke exposure on peripheral muscle through stimulation of the Nrf2 pathway and cytokines: a time-course study in mice.

Cigarette smoke (CS) exposure reduces skeletal muscle function; however, the mechanisms involved have been poorly investigated. The current study evaluated the temporal effects of aerobic exercise training on oxidant and antioxidant systems as well as inflammatory markers in skeletal muscle of mice exposed to CS. Mice were randomly allocated to control, exercise, smoke, and smoke+exercise groups and 3 time points (4, 8, and 12 weeks; n = 12 per group). Exercise training and CS exposure were performed for 30 min/day, twice a day, 5 days/week for 4, 8, and 12 weeks. Aerobic exercise improved functional capacity and attenuated the increase in the cachexia index induced by CS exposure after 12 weeks. Concomitantly, exercise training downregulated tumor necrosis factor α concentration, glutathione oxidation, and messenger RNA (mRNA) expression of Keap1 (P < 0.01) and upregulated interleukin 10 concentration, total antioxidant capacity, and mRNA expression of Nrf2, Gsr, and Txn1 (P < 0.01) in muscle. Exercise increased mRNA expression of Hmox1 compared with the control after 12 weeks (P < 0.05). There were no significant differences between smoke groups for superoxide dismutase activity and Hmox1 mRNA expression. Exercise training improved the ability of skeletal muscle to adequately upregulate key antioxidant and anti-inflammatory defenses to detoxify electrophilic compounds induced by CS exposure, and these effects were more pronounced after 12 weeks. Novelty Exercise attenuates oxidative stress in skeletal muscle from animals exposed to CS via Nrf2 and glutathione pathways. Exercise is a helpful tool to control the inflammatory balance in skeletal muscle from animals exposed to CS. These beneficial effects were evident after 12 weeks.

Time-course effects of aerobic physical training in the prevention of cigarette smoke-induced COPD.

A previous study by our group showed that regular exercise training (ET) attenuated pulmonary injury in an experimental model of chronic exposure to cigarette smoke (CS) in mice, but the time-course effects of the mechanisms involved in this protection remain poorly understood. We evaluated the temporal effects of regular ET in an experimental model of chronic CS exposure. Male C57BL/6 mice were divided into four groups: Control (sedentary + air), Exercise (aerobic training + air), Smoke (sedentary + smoke), and Smoke + Exercise (aerobic training + smoke). Mice were exposed to CS and ET for 4, 8, or 12 wk. Exercise protected mice exposed to CS from emphysema and reductions in tissue damping and tissue elastance after 12 wk (P < 0.01). The total number of inflammatory cells in the bronchoalveolar lavage increased in the Smoke group, mainly due to the recruitment of macrophages after 4 wk, neutrophils and lymphocytes after 8 wk, and lymphocytes and macrophages after 12 wk (P < 0.01). Exercise attenuated this increase in mice exposed to CS. The protection conferred by exercise was mainly observed after exercise adaptation. Exercise increased IL-6 and IL-10 in the quadriceps and lungs (P < 0.05) after 12 wk. Total antioxidant capacity and SOD was increased and TNF-α and oxidants decreased in lungs of mice exposed to CS after 12 wk (P < 0.05). The protective effects of exercise against lung injury induced by cigarette smoke exposure suggests that anti-inflammatory mediators and antioxidant enzymes play important roles in chronic obstructive pulmonary disease development mainly after the exercise adaptation.NEW & NOTEWORTHY These experiments investigated for the first time the temporal effects of regular moderate exercise training in cigarette smoke-induced chronic obstructive pulmonary disease. We demonstrate that aerobic conditioning had a protective effect in emphysema development induced by cigarette smoke exposure. This effect was most likely secondary to an effect of exercise on oxidant-antioxidant balance and anti-inflammatory mediators.

Downregulated Expression of E-cadherin and TP53 in Patients with Gastric Diseases: the Involvement of H. pylori Infection and Its Virulence Markers.

PURPOSE: Gastritis caused by infection with Helicobacter pylori is characterized by chronic inflammation and damage in gastric tissue, which is a main risk factor for gastric cancer. Associated with H. pylori, the TP53 gene tumor suppressor and the cell adhesion glycoprotein epithelial cadherin develop a relevant role in the integrity and carcinogenesis of the epithelium. We aimed to detection of H. pylori and its main virulence markers and measured the messenger RNA (mRNA) expression levels of E-cadherin and TP53 genes. METHODS: The detection of H. pylori and its virulence markers, as well as the mRNA expression levels of E-cadherin and TP53 genes, were obtained for 161 samples of gastric biopsies including 37 with normal gastric tissue, 70 with gastritis, 24 from neoplastic tissue, and 27 from adjacent non-neoplastic by means of a quantitative real-time polymerase chain reaction. RESULTS: The mRNA expression levels of E-cadherin and TP53 were found to be decreased in patients with gastritis, independently of H. pylori infection. In samples from gastric patients, the neoplastic tissue showed an accentuated decrease of expression; on the other hand, the expression of E-cadherin was normal in adjacent non-neoplastic. CONCLUSIONS: No evidence was found of the involvement of the cagA and vacA genes in the decreased expression of E-cadherin and TP53. The process of carcinogenesis is complex, and the decrease of the E-cadherin gene expression and TP53 gene expression appears to contribute significantly.

Avaliação da atividade antibacteriana do hidróxido de cálcio associado a diferentes veículos em blocos de dentina contaminados por Enterococcus faecalis / Evaluation of the antibacterial activity of calcium hydroxide associated different vehicles in dentin blocks contaminated with Enterococcus faecalis

Introdução: A infecção endodôntica ocasionada por Enterococcus faecalis é um problema sério no tratamento de dentes comprometidos. É de preocupação do cirurgião dentista um completo saneamento do sistema de canais radiculares pela aplicação de medicação antisséptica entre sessões. Dentre estas medicações, a pasta de hidróxido de cálcio tem sido associada a diferentes veículos para potencializar sua ação. Objetivos: Diante disto, este estudo objetivou avaliar e comparar a eficiência da atividade antimicrobiana in vitro de diferentes pastas de hidróxido de cálcio frente ao E. faecalis. Material e Métodos: Os testes foram executados em 49 blocos de dentina infectados com E. faecalis e tratados com pastas de hidróxido de cálcio em diferentes veículos por uma semana. A eficiência das pastas foi avaliada pela microscopia confocal de varredura a laser. Para comparação entre as pastas foi empregado o teste de Kruskal-Wallis e pelo teste de Dunn para comparações individuais com nível de significância estabelecido em 5%. Resultados: A aplicação das diferentes pastas proporcionou uma significativa alteração na proporção de bactérias viáveis e não viáveis encontradas no biovolume celular total dos blocos de dentina. Conclusão: A pasta que revelou melhor desempenho antimicrobiano foi aquela cujo veículo foi água destilada. A pasta de hidróxido de cálcio associada ao extrato propilenoglicólico de guaçatonga não apresentou desempenho antimicrobiano sobre células de E. faecalis. (AU)

Introduction: The endodontic infection caused by Enterococcus faecalis is a serious problem in the treatment of compromised teeth. It is a concern to the dental surgeon a complete sanitation of the root canal system by applying antiseptic medication between sessions. Among these medications, the calcium hydroxide paste has been linked to different vehicles to enhance its action. Objectives: Thus, this study aimed to evaluate and compare the efficiency of in vitro antimicrobial activity of different pastes of calcium hydroxide against E. faecalis. Material and Methods: Tests were performed in 49 blocks dentin infected with E. faecalis and treated with calcium hydroxide pastes in different vehicles for a week. The efficiency of the pastes was evaluated by confocal laser scanning. The Kruskal-Wallis test was used to compare the pastes and the Dunn test was used for individual comparisons with a significance level set at 5%. Results: The application of different pastes provided a significan change in the proportion of viable and non-viable bacteria found in the total cell biovolume of the blocks of dentin. Conclusion: The paste that revealed the best antimicrobial performance was the one whose vehicle was distilled water. The calcium hydroxide paste associated with the extract of guaçatonga in propylene glycol showed no antimicrobial performance on cells of E. faecalis. (AU)

Lack of association among TNF-α gene expression, -308 polymorphism (G > A) and virulence markers of Helicobacter pylori

Background Tumor necrosis factor plays a critical role in the pathogenesis of gastric diseases such as gastric cancer, and an abnormal inflammatory response has frequently been observed in dyspeptic patients. Helicobacter pylori infection can induce a gastric mucosal inflammatory response that may be influenced by -308 (G > A) polymorphisms and gene expression of theTNF-α gene. Methods One hundred and thirty-four gastric biopsy samples were collected from patients of both genders (61♂ and 73♀, mean age 40.3 ± 24.2 years) with gastric symptoms. The -308 (G > A) polymorphism of TNF-α; was characterized using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). The expression level was measured using real-time PCR, and relative quantification (RQ) was calculated using the comparative CT method (2-ΔΔCT). Results The analysis revealed an increase in TNF-α gene expression in patients with gastritis; on the other hand, no statistical differences were observed in patients with gastric cancer. In addition, no association was found among -308 polymorphism genotypes, virulence markers, or TNF-α gene expression. Conclusions Helicobacter pylori induces a large increase in TNF-α expression in patients with gastritis, regardless of tissue inflammation, but after the tissue becomes neoplastic, the presence of bacteria did not influence expression. These results suggest that the TNF-α; pathway may play an important role in the progression from gastritis to gastric cancer(AU)

Lack of association among TNF-alfa gene expression, -308 polymorphism (G > A) and virulence markers of Helicobacter pylori

Background Tumor necrosis factor plays a critical role in the pathogenesis of gastric diseases such as gastric cancer, and an abnormal inflammatory response has frequently been observed in dyspeptic patients. Helicobacter pylori infection can induce a gastric mucosal inflammatory response that may be influenced by -308 (G > A) polymorphisms and gene expression of theTNF- gene. Methods One hundred and thirty-four gastric biopsy samples were collected from patients of both genders (61 and 73, mean age 40.3 ± 24.2 years) with gastric symptoms. The -308 (G > A) polymorphism of TNF- was characterized using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). The expression level was measured using real-time PCR, and relative quantification (RQ) was calculated using the comparative CT method (2-CT). Results The analysis revealed an increase in TNF- gene expression in patients with gastritis; on the other hand, no statistical differences were observed in patients with gastric cancer. In addition, no association was found among -308 polymorphism genotypes, virulence markers, or TNF- gene expression. Conclusions Helicobacter pylori induces a large increase in TNF- expression in patients with gastritis, regardless of tissue inflammation, but after the tissue becomes neoplastic, the presence of bacteria did not influence expression. These results suggest that the TNF- pathway may play an important role in the progression from gastritis to gastric cancer.

Gene polymorphism of interleukin 1 and 8 in chronic gastritis patients infected with Helicobacter pylori.

BACKGROUND: Epidemiological investigations have indicated that Helicobacter pylori induces inflammation in the gastric mucosa regulated by several interleukins. The genes IL1B and IL8 are suggested as key factors in determining the risk of gastritis. The aim of this paper was to evaluate the association of gene polymorphism of interleukin-1 and interleukin-8 with chronic gastrits in H. pylori infected patients. A total of 60 patients underwent endoscopic procedure. Biopsy samples were collected for urease test, histopathological and molecular exams. The DNA of theses samples was extracted for detection of H. pylori and analysis of the genes mentioned above. Patients with gastritis had a higher frequency of H. pylori-positive samples. RESULTS: H. pylori was detected in 30/60 patients (50%) by PCR. As for polymorphism of interleukin 8 (-251) gene we observed a statistical difference when analyzed TA (p = 0.039) and TT (p = 0.047) genotypes. In the IL1B31 there was a statistical difference in TT (p = 0.01) genotype and in the IL1B-511 there wasn't any statistical difference. CONCLUSION: Our results suggest a strong correlation between the presence of chronic gastritis and infection by H. pylori and that IL1B-31TT and IL8-251TT genotypes appear to act as protective factors against H. pylori infection while IL8-251TA genotype may comprise a risk factor for infection with this bacterium.

Association among H. pylori virulence markers dupA, cagA and vacA in Brazilian patients

Only a few Helicobacter pylori-infected individuals develop severe gastric diseases and virulence factors of H. pylori appear to be involved in such clinical outcomes. Duodenal ulcer promoting gene A (dupA) is a novel virulence factor of Helicobacter pylori that is associated with duodenal ulcer development and reduced risk for gastric carcinoma in some populations. The aims of the present study were to determine the presence of dupA gene and evaluate the association among dupA and other virulence factors including cagA and vacA in Brazilian patients. Gastric biopsies were obtained from 205 dyspeptic patients (100 children and 105 adults). DNA was extracted and analyzed for the presence of H. pylori and its virulence factors using the polymerase chain reaction method.

Gene polymorphism of interleukin 1 and 8 in chronic gastritis patients infected with Helicobacter pylori

Epidemiological investigations have indicated that Helicobacter pylori induces inflammation in the gastric mucosa regulated by several interleukins. The genes IL1B and IL8 are suggested as key factors in determining the risk of gastritis. The aim of this paper was to evaluate the association of gene polymorphism of interleukin-1 and interleukin-8 with chronic gastrits in H. pylori infected patients. A total of 60 patients underwent endoscopic procedure. Biopsy samples were collected for urease test, histopathological and molecular exams. The DNA of theses samples was extracted for detection of H. pylori and analysis of the genes mentioned above. Patients with gastritis had a higher frequency of H. pylori-positive samples.

Association among H. pylori virulence markers dupA, cagA and vacA in Brazilian patients

Only a few Helicobacter pylori-infected individuals develop severe gastric diseases and virulence factors of H. pylori appear to be involved in such clinical outcomes. Duodenal ulcer promoting gene A (dupA) is a novel virulence factor of Helicobacter pylori that is associated with duodenal ulcer development and reduced risk for gastric carcinoma in some populations. The aims of the present study were to determine the presence of dupA gene and evaluate the association among dupA and other virulence factors including cagA and vacA in Brazilian patients. Gastric biopsies were obtained from 205 dyspeptic patients (100 children and 105 adults). DNA was extracted and analyzed for the presence of H. pylori and its virulence factors using the polymerase chain reaction method.

Gene polymorphism of interleukin 1 and 8 in chronic gastritis patients infected with Helicobacter pylori

Epidemiological investigations have indicated that Helicobacter pylori induces inflammation in the gastric mucosa regulated by several interleukins. The genes IL1B and IL8 are suggested as key factors in determining the risk of gastritis. The aim of this paper was to evaluate the association of gene polymorphism of interleukin-1 and interleukin-8 with chronic gastrits in H. pylori infected patients. A total of 60 patients underwent endoscopic procedure. Biopsy samples were collected for urease test, histopathological and molecular exams. The DNA of theses samples was extracted for detection of H. pylori and analysis of the genes mentioned above. Patients with gastritis had a higher frequency of H. pylori-positive samples.

Polimorfismo da Interleucina-8 -251T>A e Helicobacter pylori / Interleukin-8 -251T>A polymorphism and Helicobacter pylori

Introdução: o Helicobacter pylori é um importante patógeno associado ao desenvolvimento de gastrite crônica, úlcera péptica e doenças gástricas. Vários autores relataram que a infiltração de células inflamatórias, incluindo neutrófilos, é um traço da patologia da mucosa gástrica associada com a infecção. Há evidências de que a inflamação está associada à gravidade das lesões gástricas. A interleucina 8 (IL-8), um membro da família das citocinas, é um ativador quimiotático de neutrófilos e linfócitos e tem sido descrito que o aumento dos níveis de IL-8 na mucosa gástrica pode estar associado com a infecção por H.pylori. Objetivos: os objetivos deste trabalho foram (i) caracterizar o polimorfismo da Interleucina-8 -251T>A (ii) e verificar a possível relação entre este polimorfismo e infecção por H.pylori. Métodos: cento e sessenta pacientes sintomáticos (com idade média de 48,7 anos) participaram do estudo: 107 pacientes positivos para H.pylori e 53 negativos, previamente diagnosticados por PCR. Os genótipos da IL-8 -251 T>A foram determinados através da reação em cadeia da polimerase (PCR) e utilização de enzimas de restrição (RFLP). Resultados e Conclusões: nossos resultados indicam que não há associação entre o polimorfismo da IL-8 -251 T>A e a infecção por H.pylori ou pelo gênero dos pacientes.

Background: Helicobacter pylori is an important pathogen associated with the development of chronic gastritis, peptic ulcer disease and gastric disease. Several authors reported that the infiltration of inflammatory cells, including neutrophils is the trace of the pathology of gastric mucosa, associated with the infection. There is high evidence that inflammation is associated with severity of gastric lesions. Interleukin-8 (IL-8), a member of cytokines family, is an activator and chemoattractant of neutrophils and lymphocytes. It has been reported that increased gastric mucosal levels of IL-8 is associated with H. pylori infection. Objective: the objectives of this paper were (i) characterize Interleukin-8 -251T>A polymorphism and (ii) to examine the possible relationship between this polymorphism and the H. pylori infection. Methods: one hundred and sixty patients, (with a mean age 48.7 years) presenting recurrent abdominal pain participated in the study: 107 H. pylori positives and 53 H. pylori negatives previously diagnosed by PCR. IL8 -251T>A genotypes were determined using a polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). Results and Conclusions: our findings indicate that there is no association of IL-8 -251T>A with H. pylori-infected patients or gender of these patients and these conclusions were consistent with other reports from different population samples.