Catecholamine-Directed epithelial cell interactions with bacteria in the intestinal mucosa

Research output: Chapter in Book/Report/Conference proceedingChapter

7 Scopus citations

Abstract

The catecholamines epinephrine, norepinephrine and dopamine are present in or have access to mucous membranes in the digestive, respiratory and genitourinary tracts, which represent the first sites of microbial colonization and infection within the body. Epithelial cells at mucosal surfaces establish and maintain symbiotic microbial communities and serve as the initial cellular point of contact for pathogens with the animal host. These cells express receptors that are capable of detecting and responding to microbe-associated molecular patterns and in most host species express G protein-coupled receptors for catecholamines. Although it is increasingly recognized that substances produced and released from nerves and endocrine cells can exert immuno-modulatory actions at mucosal sites, there have been few investigations focused specifically on the catecholaminergic modulation of interactions between the mucosal epithelium and bacteria or other mucosaassociated microorganisms. The potential biomedical importance of this phenomenon cannot be understated. For example, psychological stress or other conditions that activate the sympathetic nervous system to release epinephrine and norepinephrine may act to produce short-term changes in luminal and mucosal microbial communities or alter the course of a bacterial infection. This chapter will briefly review this developing and important research area of mucosa-microbe interactions with a focus on intestinal host defense.

Original languageEnglish (US)
Title of host publicationAdvances in Experimental Medicine and Biology
PublisherSpringer New York LLC
Pages79-99
Number of pages21
DOIs
StatePublished - 2016

Publication series

NameAdvances in Experimental Medicine and Biology
Volume874
ISSN (Print)0065-2598
ISSN (Electronic)2214-8019

Bibliographical note

Publisher Copyright:
© Springer International Publishing AG 2016.

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