Dysbiotic Proteobacteria expansion: a microbial signature of epithelial dysfunction
[Display omitted] •Epithelial hypoxia drives anaerobiosis to maintain dominance of obligate anaerobes.•Increased epithelial oxygenation disrupts anaerobiosis in the large intestine.•Elevated oxygen availability drives a shift from obligate to facultative anaerobes.•Proteobacteria expansion is a micr...
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Published in: | Current opinion in microbiology Vol. 39; pp. 1 - 6 |
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Main Authors: | , , , |
Format: | Journal Article |
Language: | English |
Published: |
England
Elsevier Ltd
01-10-2017
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Online Access: | Get full text |
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Summary: | [Display omitted]
•Epithelial hypoxia drives anaerobiosis to maintain dominance of obligate anaerobes.•Increased epithelial oxygenation disrupts anaerobiosis in the large intestine.•Elevated oxygen availability drives a shift from obligate to facultative anaerobes.•Proteobacteria expansion is a microbial signature of colonic epithelial dysfunction.
A balanced gut microbiota is important for health, but the mechanisms maintaining homeostasis are incompletely understood. Anaerobiosis of the healthy colon drives the composition of the gut microbiota towards a dominance of obligate anaerobes, while dysbiosis is often associated with a sustained increase in the abundance of facultative anaerobic Proteobacteria, indicative of a disruption in anaerobiosis. The colonic epithelium is hypoxic, but intestinal inflammation or antibiotic treatment increases epithelial oxygenation in the colon, thereby disrupting anaerobiosis to drive a dysbiotic expansion of facultative anaerobic Proteobacteria through aerobic respiration. These observations suggest a dysbiotic expansion of Proteobacteria is a potential diagnostic microbial signature of epithelial dysfunction, a hypothesis that could spawn novel preventative or therapeutic strategies for a broad spectrum of human diseases. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 1369-5274 1879-0364 |
DOI: | 10.1016/j.mib.2017.07.003 |