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Life Sci. 2018 Dec 15;215:145-151. doi: 10.1016/j.lfs.2018.11.009. Epub 2018 Nov 7.

Contribution of sulfate-reducing bacteria to homeostasis disruption during intestinal inflammation.

Author information

1
Instituto de Biofísica Carlos Chagas Filho - IBCCF, Universidade Federal do Rio de Janeiro, RJ, Brazil; LITEB, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, RJ, Brazil; Department of Pediatrics, University of Arizona, Tucson, AZ, USA.
2
Instituto de Biofísica Carlos Chagas Filho - IBCCF, Universidade Federal do Rio de Janeiro, RJ, Brazil.
3
Departamento de Biologia Celular e Molecular, Instituto de Biologia, Universidade Federal Fluminense, Niteroi, RJ, Brazil; LITEB, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, RJ, Brazil. Electronic address: laramelo@yahoo.com.br.

Abstract

Alteration in microbial populations and metabolism are key events associated with disruption of intestinal homeostasis and immune tolerance during intestinal inflammation. A substantial imbalance in bacterial populations in the intestine and their relationships with the host have been observed in patients with inflammatory bowel disease (IBD), believed to be part of an intricate mechanism of triggering and progression of intestinal inflammation. Because elevated numbers of sulfate-reducing bacteria (SRB) have been found in the intestines of patients with IBD, the study of their interaction with intestinal cells and their potential involvement in IBD has been the focus of investigation to better understand the intestinal pathology during IBD, as well as to find new ways to treat the disease. SRB not only directly interact with intestinal epithelial cells during intestinal inflammation but may also promote intestinal damage through generation of hydrogen sulfide at high levels. Herein we review the literature to discuss the various aspects of SRB interaction with host intestinal tissue, focusing on their interaction with intestinal epithelial and immune cells during intestinal inflammation.

KEYWORDS:

Dysbiosis; Epithelial cells; H(2)S; Inflammation; SRB

PMID:
30414430
DOI:
10.1016/j.lfs.2018.11.009
[Indexed for MEDLINE]

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