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Stress at the intestinal surface: catecholamines and mucosa-bacteria interactions

Journal

CELL AND TISSUE RESEARCH
Volume 343, Issue 1, Pages 23-32

Publisher

SPRINGER
DOI: 10.1007/s00441-010-1050-0

Keywords

Bacteria; Autonomic nervous system; Immune cells; Nerves; Gut-to-brain

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Funding

  1. National Institutes of Health [DA-17236, DA-10200]
  2. NATIONAL INSTITUTE ON DRUG ABUSE [R01DA010200, K01DA017236] Funding Source: NIH RePORTER

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Psychological stress has profound effects on gastrointestinal function, and investigations over the past few decades have examined the mechanisms by which neural and hormonal stress mediators act to modulate gut motility, epithelial barrier function and inflammatory states. With its cellular diversity and large commensal bacterial population, the intestinal mucosa and its overlying mucous environment constitute a highly interactive environment for eukaryotic host cells and prokaryotic bacteria. The elaboration of stress mediators, particularly norepinephrine, at this interface influences host cells engaged in mucosal protection and the bacteria which populate the mucosal surface and gut lumen. This review will address growing evidence that norepinephrine and, in some cases, other mediators of the adaptation to stress modulate mucosal interactions with enteric bacteria. Stress-mediated changes in this delicate interplay may shift the microbial colonization patterns on the mucosal surface and alter the susceptibility of the host to infection. Moreover, changes in host-microbe interactions in the digestive tract may also influence ongoing neural activity in stress-responsive brain areas.

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