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Diet and microbiota in inflammatory bowel disease: The gut in disharmony

World Journal of Gastroenterology 2017年第12期23卷 2124-2140页

作者： Davy CM Rapozo claudio bernardazzi Heitor Siffert Pereira de Souza Coordenacao de Pesquisa Instituto Nacional de Cancer Servico de Gastroenterologia e Laboratório Multidisciplinar de Pesquisa Departamento de Clínica MédicaHospital Universitário Clementino Fraga FilhoUniversidade Federal do Rio de Janeiro D’Or Institute for Research and Education Rua Diniz Cordeiro 30BotafogoRio de JaneiroRJ 22281-100Brazil

Bacterial colonization of the gut shapes both the local and the systemic immune response and is implicated in the modulation of immunity in both healthy and disease states. Recently, quantitative and qualitative changes in the composition of the gut microbiota have been detected in Crohn's disease and ulcerative colitis, reinforcing the hypothesis of dysbiosis as a relevant mechanism underlying inflammatory bowel disease(IBD) pathogenesis. Humans and microbes have coexisted and co-evolved for a long time in a mutually beneficial symbiotic association essential for maintaining homeostasis. However, the microbiome is dynamic, changing with age and in response to environmental modifications. Among such environmental factors, food and alimentary habits, progressively altered in modern societies, appear to be critical modulators of the microbiota, contributing to or co-participating in dysbiosis. In addition, food constituents such as micronutrients are important regulators of mucosal immunity, with direct or indirect effects on the gut microbiota. Moreover, food constituents have recently been shown to modulate epigenetic mechanisms, which can result in increased risk for the development and progression of IBD. Therefore, it is likely that a better understanding of the role of different food components in intestinal homeostasis and the resident microbiota will be essential for unravelling the complex molecular basis of the epigenetic, genetic and environment interactions underlying IBD pathogenesis as well as for offering dietary interventions with minimal side effects.

关键词： Diet Microbiota Epigenetics Crohn’s disease Ulcerative colitis

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Damage-associated molecular patterns in inflammatory bowel disease:From biomarkers to therapeutic targets

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World Journal of Gastroenterology 2018年第41期24卷 4622-4634页

作者： Hayandra Ferreira Nanini claudio bernardazzi Fernando Castro Heitor Siffert Pereira de Souza Servico de Gastroenterologia e Laboratorio Multidisciplinar de Pesquisa Departamento de Clinica MedicaHospital Universitario Clementino Fraga FilhoUniversidade Federal do Rio de JaneiroRio de JaneiroRJ 21941-913Brazil D’Or Institute for Research and Education(IDOR) Rua Diniz Cordeiro 30BotafogoRio de JaneiroRJ 22281-100Brazil

The chronic inflammatory process underlying inflammatory bowel disease (IBD), comprising Crohn's disease and ulcerative colitis, derives from the interplay of several components in a genetically susceptible host. These components include environmental elements and gut microbiota a dysbiosis. For decades, immune abnormalities have been investigated as critically important in IBD pathogenesis, and attempts to develop effective therapies have predominantly targeted the immune system. Nevertheless, immune events represent only one of the constituents contributing to IBD pathogenesis within the context of the complex cellular and molecular network underlying chronic intestinal inflammation. These factors need to be appreciated within the milieu of nonimmune components. Damage-associated molecular patterns (DAMPs), which are essentially endogenous stress proteins expressed or released as a result of cell or tissue damage, have been shown to act as direct proinflammatory mediators. Excessive or persistent signalling mediated by such molecules can underlie several chronic inflammatory disorders, including IBD. The release of endogenous DAMPs amplifies the inflammatory response driven by immune and non-immune cells and promotes epigenetic reprogramming in IBD.The effects determine pathologic changes,which may sustain chronic intestinal inflammation and also underlie specific disease phenotypes.In addition to highlighting the potential use of DAMPs such as calprotectin as biomarkers,research on DAMPs may reveal novel mechanistic associations in IBD pathogenesis and is expected to uncover putative therapeutic targets.

关键词： Damage-associated molecular patterns Environmental factors Epigenetics Inflammatory bowel disease Therapeutic targets

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