Helicobacter pylori may participate in the development of inflammatory bowel disease by modulating the intestinal microbiota / 中华医学杂志(英文版)

Inflammatory bowel disease (IBD) is a non-specific inflammatory disease of the gastrointestinal (GI) tract that is generally accepted to be closely related to intestinal dysbiosis in the host. GI infections contribute a key role in the pathogenesis of IBD; however, although the results of recent clinical studies have revealed an inverse correlation between Helicobacter pylori (H. pylori) infection and IBD, the exact mechanism underlying the development of IBD remains unclear. H. pylori, as a star microorganism, has been a focus for decades, and recent preclinical and real-world studies have demonstrated that H. pylori not only affects the changes in the gastric microbiota and microenvironment but also influences the intestinal microbiota, indicating a potential correlation with IBD. Detailed analysis revealed that H. pylori infection increased the diversity of the intestinal microbiota, reduced the abundance of Bacteroidetes, augmented the abundance of Firmicutes, and produced short-chain fatty acid-producing bacteria such as Akkermansia. All these factors may decrease vulnerability to IBD. Further studies investigating the H. pylori-intestinal microbiota metabolite axis should be performed to understand the mechanism underlying the development of IBD.

Correlation between Vitamin D Status and Gut Microbiota in Patients with Inflammatory Bowel Disease / 中国医学科学院学报

Objective To investigate the correlation between serum total 25-hydroxyvitamin D[T-25(OH)D]level and fecal microbiota in patients with inflammatory bowel disease(IBD). Methods Twenty-three patients with IBD completed the tests for serum T-25(OH)D,and the fecal microbiota was studied using V4 hypervariable region of 16S ribosomal RNA(rRNA)gene sequencing.According to serum T-25(OH)D level,the patients were divided into three groups including vitamin D normal group(

Presence of Mycobacterium avium subsp. paratuberculosis (MAP) in Brazilian patients with inflammatory bowel diseases and in controls / Presença de Mycobacterium avium subsp. paratuberculosis (MAP) em pacientes brasileiros com doença inflamatória intestinal e em controles

CONTEXT AND OBJECTIVE: Mycobacterium avium subsp. paratuberculosis (MAP) has attracted the interest of researchers because of similarities between paratuberculosis and Crohn's disease (CD). The aim of this study was to evaluate the frequency of MAP through cultures, histology and polymerase chain reaction (PCR) on intestinal biopsies from Brazilian CD patients. Quantitative real time PCR (qRT-PCR) was performed on positive samples. DESIGN AND SETTING: Analytical cross-sectional study with control group at two federal universities. METHODS: Fresh samples were collected from 25 patients; five with CD, eight with ulcerative colitis (UC) and 12 controls with non-inflammatory bowel disease (nIBD). Formalin-fixed paraffin-embedded (FFPE) samples from 143 patients were also collected: 44 CD, 49 UC and 56 nIBD. RESULTS: None of the fresh samples was positive for MAP. Five FFPE samples (one CD, two UC and two nIBD) and three fresh samples (one in each group) were positive through IS900-PCR. qRT-PCR was performed on these eight samples. Among the FFPE samples, there were 192.12 copies/μl in the CD group, 72.28 copies/μl in UC and 81.43 copies/μl in nIBD. Among the fresh samples, there were 432.99 copies/μl, 167.92 copies/μl and 249.73 copies/μl in the CD, UC and nIBD groups, respectively. The highest bacterial load was in the CD group. CONCLUSION: This study does not provide evidence for a role of MAP in the etiology of CD, although MAP DNA was detected in all three patient groups. This is the first report of MAP presence in human intestinal biopsies in Brazil.

CONTEXTO E OBJETIVO: Mycobaterium avium subsp. paratuberculosis (MAP) tem atraído o interesse de pesquisadores devido às semelhanças entre a paratuberculose e a doença de Crohn (CD). Este estudo objetivou avaliar a frequência de MAP por meio de cultura, histologia e reação da polimerase em cadeia (PCR), em biópsias intestinais de pacientes brasileiros com CD. PCR quantitativa em tempo real (qRT-PCR) foi realizada nas amostras positivas. TIPO DE ESTUDO E LOCAL: Estudo transversal analítico com grupo controle realizado em duas universidades federais. MÉTODOS: Amostras frescas foram coletadas de 25 pacientes; cinco com CD, oito com colite ulcerativa (UC) e 12 controles sem doença inflamatória intestinal (nIBD). Também foram coletadas 149 amostras fixadas em parafina (FFPE): 44 CD, 49 UC e 56 nIBD. RESULTADOS: Nenhuma das amostras frescas foi positiva para MAP. Cinco amostras FFPE (uma CD, duas UC e duas nIBD) e três amostras frescas (uma de cada grupo) foram positivas por IS900-PCR. qRT-PCR foi realizada nessas oito amostras. Nas amostras FFPE, havia 192,12 cópias/μl no grupo CD, 72,28 cópias/μl no UC e 81,43 cópias/μl no nIBD. Nas amostras frescas, havia 432,99 cópias/μl, 167,92 cópias/μl e 249,73 cópias/μl nos grupos CD, UC e nIBD, respectivamente. A maior carga bacteriana foi encontrada no grupo CD. CONCLUSÃO: Este estudo não fornece evidências do papel de MAP na etiologia da CD, embora DNA de MAP tenha sido detectado em pacientes dos três grupos. Este é o primeiro relato da presença de MAP em biópsias intestinais humanas no Brasil.

Fusobacterium Isolates Recovered From Colonic Biopsies of Inflammatory Bowel Disease Patients in Korea

No abstract available.

Terapia nutricional nas doenças inflamatórias intestinais: artigo de revisão / Nutrition therapy in inflammatory bowel diseases: review article

OBJECTIVE: This article aims to discuss the role of nutrition therapy in Inflammatory Bowel Diseases according to its indications, contraindications, and the as main results obtained with prebiotics, probiotics, symbiotics and other nutritional interventions. Data source: We performed a literature review using the databases Pubmed, Scielo and Lilacs. Data synthesis: Inflammatory Bowel Diseases are chronic illnesses that affect primarily the gastrointestinal tract and are divided in two most common forms of presentation: Crohn's Disease and Ulcerative Colitis. The chronic inflammation can cause intestinal lesions, anorexia, nutrients malabsorption, oxidative stress and higher energy consumption, increasing the risk of malnutrition. Nutritional status is directly associated with the disease severity and malnutrition is a serious complication of inflammatory bowel diseases that worsens the patients' prognosis. Nutritional therapy is used to prevent or treat the malnutrition, to correct macro and micronutrients deficits and to reverse some of the metabolic and pathological consequences of these diseases. In the majority of patients, the nutrition therapy has an adjuvant role combined to medical or surgical treatments, but in some specific situations it can be the main treatment. CONCLUSIONS: Despite the benefits of nutritional therapy, more meta-analysis and double-blind controlled studies about these diseases are required to assure the good results obtained in some of the published trials.

OBJETIVO: O objetivo do artigo é discutir o papel da Terapia Nutricional nas Doenças Inflamatórias Intestinais de acordo com suas indicações e contraindicações, bem como os principais resultados com prebióticos, probióticos, simbióticos e outras intervenções nutricionais nessas doenças. Fonte dos dados: Foi realizada busca por artigos nas bases de dados: Pubmed, Scielo e Lilacs. Síntese dos dados: Doenças Inflamatórias Intestinais são doenças crônicas que acometem principalmente o trato gastrointestinal e se dividem em duas formas mais comuns de apresentação: Doença de Crohn e Retocolite Ulcerativa. A inflamação crônica pode causar lesões intestinais, anorexia, má absorção de nutrientes, estresse oxidativo e aumento do gasto energético, aumentando o risco de desnutrição. O estado nutricional está diretamente associado com a gravidade da doença e a desnutrição é uma complicação que piora o prognóstico do paciente. A terapia nutricional é utilizada para impedir ou corrigir a desnutrição, repor deficiências de macro e micronutrientes e reverter parte das consequências metabólicas patológicas dessas doenças. Na maior parte dos pacientes, a terapia nutricional atua como coadjuvante combinada ao tratamento clínico ou cirúrgico, mas em algumas situações específicas pode ser o principal tratamento. CONCLUSÃO: Apesar dos vários benefícios atingidos pelo uso da terapia nutricional, mais metanálises e estudos randomizados duplo cegos ainda são necessários para comprovar os efeitos de suplementos específicos, garantindo, dessa maneira, resultados positivos na sua aplicação

Fecal transplantation: passing fashion or here to stay?

Several trillions of bacteria, distributed among more than 1,000 species, are natural inhabitants of the human intestinal tract and constitute what is now known as the gut microbiota. Although its composition varies within and between individuals with age, diet, and health status, it is becoming increasingly recognized that imbalances in the bacterial microbiota (dysbiosis) are linked to a number of conditions such as antibiotic-associated diarrhea, inflammatory bowel disease, and obesity, among others. Fecal transplantation where a preparation of stool from a microbiologically screened donor is administered into the colon of an affected recipient has been shown to be highly effective for the treatment of recurrent Clostridium difficile infection. Several trials of this therapy are now underway for gut dysbiosis in a number of patient disease groups raising concerns on the risk of transmission of infectious agents from donor to recipient, possible long-term adverse consequences of treatment, and effective regulation of the stool material used for the procedure. A worrying aspect is the emergence of private stool banks providing samples to the general public for self-administration.

Colitis y trasplante de microflora intestinal: ¿cuándo plantearlo? / Colitis and fecal microbiota transplantation: who benefits?

The gastrointestinal microbiota acts as a metabolic organ that provides enzymatic pathways, contributes to the development and maintenance of local and systemic lymphoid organs, regulates the homeostasis of the intestinal epithelial barrier, modulates the systemic inflammatory and metabolic processes and activates the immune system, providing protection against bacterial and viral agents. Clostridium difficile diarrhea is the leading cause of nosocomial diarrhea with high morbidity and mortality rates. This occurs, among other causes, due to dysbiosis. Fecal microflora transplantation is an option, particularly in recurrent episodes. There are case reports on fecal microflora transplantation used for the treatment of inflammatory bowel disease, with promising results.

La microbiota gastrointestinal funciona como un órgano metabólico que provee de rutas enzimáticas no presentes en nuestro organismo; contribuye al desarrollo y mantenimiento de órganos linfoides locales y sistémicos, a la homeostasis de la barrera epitelial intestinal; modula los procesos inflamatorios sistémicos y metabólicos y activa el sistema inmunológico sitémico, brindando protección frente agresiones bacterianas y virales. La diarrea por Clostridium difficile es la principal causa de diarrea intrahospitalaria con una alta morbilidad y mortalidad. Esta se produce entre otras causas por una disbiosis. El trasplante de microflora fecal ha demostrado ser una opción terapéutica eficaz, especialmente en los episodios recurrentes. Existen reportes de casos con resultados promisorios en que se utiliza el trasplante de microflora fecal para el tratamiento de enfermedad inflamatoria intestinal crónica.

Infecciones en la patogenia de la enfermedad inflamatoria intestinal / Infections in the pathogeny of inflammatory bowel disease

La enfermedad inflamatoria intestinal (EII) es una entidad compleja. Su desarrollo requiere de la interacción entre factores ambientales y la flora gastrointestinal, en un individuo genéticamente susceptible. Nuestro aparato gastrointestinal es un extraordinario, complejo y dinámico modelo de simbiosis o mutualismo con la flora. Los factores ambientales como el tabaco, las infecciones gastrointestinales y los antiinflamatorios no esteroidales juegan probablemente un rol iniciador y/o modificador de la enfermedad. La mucosa intestinal tiene la difícil tarea de limitar la respuesta inflamatoria contra la flora y de mantener la habilidad de generar una respuesta inmune contra los microorganismos patógenos. Esto crea una relación de equilibrio dinámico y frágil que al alterarse cualquiera de sus componentes puede generar un proceso inflamatorio. Existe evidencia que las infecciones pueden tener un rol tanto en el inicio de la enfermedad como en las reagudizaciones de ésta. Es así como las infecciones bacterianas gastrointestinales agudas y la Escherichia coli adherente invasora confieren un riesgo para desarrollar una enfermedad inflamatoria intestinal. Para Mycobacterium avium subespecie paratuberculosis (MAP) sólo se ha establecido una asociación y no un rol patogénico. Por último ha aumentado la incidencia y morbimortalidad de la infección por Clostridium difficile en los pacientes con EII.

Infections in the pathogeny of inflammatory bowel disease Inflammatory bowel disease (IBD) is a complex entity. Its development requires the interaction between environmental factors and gastrointestinal flora in a genetically susceptible subject. Our gastrointestinal tract is an extraordinary, complex and dynamic model of symbiosis or mutualism with the flora. Environmental factors such as tobacco, gastrointestinal infections and non-steroidal anti-inflammatory drugs might play a role of starter and/or modifier of the disease. The intestinal mucosa has the difficult task of limiting the inflammatory response against the flora and of keeping the capability of generating an immune response against pathogenic microorganisms. This creates a dynamic equilibrium relation that is fragile, and that when any of its components is altered, it can cause an inflammatory process. There is evidence that infections can have a role both in the beginning and in the episodes of New-Rebounds of the disease. Therefore, acute gastrointestinal bacterial infections and adherent-invasive Escherichia coli pose a risk of developing an inflammatory bowel disease. In the case of Mycobacterium avium subspecies paratuberculosis (MAP) an association has been established, but not a pathogenic role. The incidence and morbimortality of Clostridium difficile infection has increased in patients with IBD.

Inflammatory Bowel Diseases and Enteric Microbiota / 대한소화기학회지

Intestinal mucosal layers are colonized by a complex microbiota that provides beneficial effects under normal physiological conditions, but is capable of contributing to chronic inflammatory disease such as inflammatory bowel disease (IBD) in susceptible individuals. Studies have shown that the enteric microbiota may drive the development of the gut immune system and can induce immune homeostasis as well as contribute to the development of IBD although the precise etiology is still unknown. Therefore, intestinal microbes seem to play a key role in the disease pathogenesis. Especially, dysbiosis, which is a shift in the composition of enteric microbiota to a nonphysiologic composition, is associated with one or more defects in mucosal immune functions, including microbe recognition, barrier function, intercellular communication, and anti-microbial effector mechanisms. This review focuses on the impact of enteric microbiota on the development and perpetuation of IBD. In addition, interactions with enteric bacteria and mucosal cells, including intestinal epithelial cells, dendritic cells, and T cells, to induce immune responses at mucosal surfaces have been discussed in the point of IBD pathogenesis. Further extension of the knowledge of enteric microbiota may lead to insights on the pathogenesis and new therapeutic strategies for IBD.

Good bug, bad bug: in the case of enteric inflammatory disease does the epithelium decide?

Many studies demonstrate that intestinal inflammation is either initiated or exaggerated by a component of the normal microbiota, most likely commensal bacteria or products derived from these organisms. We review the nature of human inflammatory bowel disease, the evidence for the involvement of the normal bacterial flora in these disorders and the relevance of maintaining the integrity of the epithelial barrier. Moreover, we, and others, have shown abnormal mitochondria structure in tissue resections from patients with inflammatory bowel disease and tissues from rodents that demonstrated psychological stress-induced increases in epithelial permeability. Thus, we also consider the possibility that a defect in epithelial mitochondrial function would predispose an individual to respond to their commensal bacteria flora - no longer considering them as a beneficial passive inhabitant, but rather perceiving them as a threatening and pro-inflammatory stimulus. In support of this postulate, we discuss our recent findings from an in vitro model showing that the human colon-derived T84 cell line exposed to the metabolic stressor, dinitrophenol, and the non-pathogenic, non-invasive, Escherichia coli (strain HB101) display a loss of barrier function, increased signal transduction and increased production of the chemokine, interleukin 8.