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Vasoactive intestinal peptide ameliorates intestinal barrier disruption associated with Citrobacter rodentium-induced colitis.
Am J Physiol Gastrointest Liver Physiol. 2009 Oct; 297(4):G735-50.AJ

Abstract

Attaching and effacing bacterial pathogens attach to the apical surface of epithelial cells and disrupt epithelial barrier function, increasing permeability and allowing luminal contents access to the underlying milieu. Previous in vitro studies demonstrated that the neuropeptide vasoactive intestinal peptide (VIP) regulates epithelial paracellular permeability, and the high concentrations and close proximity of VIP-containing nerve fibers to intestinal epithelial cells would support such a function in vivo. The aim of this study was to examine whether VIP treatment modulated Citrobacter rodentium-induced disruption of intestinal barrier integrity and to identify potential mechanisms of action. Administration of VIP had no effect on bacterial attachment although histopathological scoring demonstrated a VIP-induced amelioration of colitis-induced epithelial damage compared with controls. VIP treatment prevented the infection-induced increase in mannitol flux a measure of paracellular permeability, resulting in levels similar to control mice, and immunohistochemical studies demonstrated that VIP prevented the translocation of tight junction proteins: zonula occludens-1, occludin, and claudin-3. Enteropathogenic Escherichia coli (EPEC) infection of Caco-2 monolayers confirmed a protective role for VIP on epithelial barrier function. VIP prevented EPEC-induced increase in long myosin light chain kinase (MLCK) expression and myosin light chain phosphorylation (p-MLC). Furthermore, MLCK inhibition significantly attenuated bacterial-induced epithelial damage both in vivo and in vitro. In conclusion, our results indicate that VIP protects the colonic epithelial barrier by minimizing bacterial-induced redistribution of tight junction proteins in part through actions on MLCK and MLC phosphorylation.

Authors+Show Affiliations

Division of Gastroenterology, Child and Family Research Institute, BC Children's Hospital, Vancouver, BC, Canada.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19661153

Citation

Conlin, V S., et al. "Vasoactive Intestinal Peptide Ameliorates Intestinal Barrier Disruption Associated With Citrobacter Rodentium-induced Colitis." American Journal of Physiology. Gastrointestinal and Liver Physiology, vol. 297, no. 4, 2009, pp. G735-50.
Conlin VS, Wu X, Nguyen C, et al. Vasoactive intestinal peptide ameliorates intestinal barrier disruption associated with Citrobacter rodentium-induced colitis. Am J Physiol Gastrointest Liver Physiol. 2009;297(4):G735-50.
Conlin, V. S., Wu, X., Nguyen, C., Dai, C., Vallance, B. A., Buchan, A. M., Boyer, L., & Jacobson, K. (2009). Vasoactive intestinal peptide ameliorates intestinal barrier disruption associated with Citrobacter rodentium-induced colitis. American Journal of Physiology. Gastrointestinal and Liver Physiology, 297(4), G735-50. https://doi.org/10.1152/ajpgi.90551.2008
Conlin VS, et al. Vasoactive Intestinal Peptide Ameliorates Intestinal Barrier Disruption Associated With Citrobacter Rodentium-induced Colitis. Am J Physiol Gastrointest Liver Physiol. 2009;297(4):G735-50. PubMed PMID: 19661153.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Vasoactive intestinal peptide ameliorates intestinal barrier disruption associated with Citrobacter rodentium-induced colitis. AU - Conlin,V S, AU - Wu,X, AU - Nguyen,C, AU - Dai,C, AU - Vallance,B A, AU - Buchan,A M J, AU - Boyer,L, AU - Jacobson,K, Y1 - 2009/08/06/ PY - 2009/8/8/entrez PY - 2009/8/8/pubmed PY - 2010/10/27/medline SP - G735 EP - 50 JF - American journal of physiology. Gastrointestinal and liver physiology JO - Am J Physiol Gastrointest Liver Physiol VL - 297 IS - 4 N2 - Attaching and effacing bacterial pathogens attach to the apical surface of epithelial cells and disrupt epithelial barrier function, increasing permeability and allowing luminal contents access to the underlying milieu. Previous in vitro studies demonstrated that the neuropeptide vasoactive intestinal peptide (VIP) regulates epithelial paracellular permeability, and the high concentrations and close proximity of VIP-containing nerve fibers to intestinal epithelial cells would support such a function in vivo. The aim of this study was to examine whether VIP treatment modulated Citrobacter rodentium-induced disruption of intestinal barrier integrity and to identify potential mechanisms of action. Administration of VIP had no effect on bacterial attachment although histopathological scoring demonstrated a VIP-induced amelioration of colitis-induced epithelial damage compared with controls. VIP treatment prevented the infection-induced increase in mannitol flux a measure of paracellular permeability, resulting in levels similar to control mice, and immunohistochemical studies demonstrated that VIP prevented the translocation of tight junction proteins: zonula occludens-1, occludin, and claudin-3. Enteropathogenic Escherichia coli (EPEC) infection of Caco-2 monolayers confirmed a protective role for VIP on epithelial barrier function. VIP prevented EPEC-induced increase in long myosin light chain kinase (MLCK) expression and myosin light chain phosphorylation (p-MLC). Furthermore, MLCK inhibition significantly attenuated bacterial-induced epithelial damage both in vivo and in vitro. In conclusion, our results indicate that VIP protects the colonic epithelial barrier by minimizing bacterial-induced redistribution of tight junction proteins in part through actions on MLCK and MLC phosphorylation. SN - 1522-1547 UR - https://www.unboundmedicine.com/medline/citation/19661153/Vasoactive_intestinal_peptide_ameliorates_intestinal_barrier_disruption_associated_with_Citrobacter_rodentium_induced_colitis_ L2 - https://journals.physiology.org/doi/10.1152/ajpgi.90551.2008?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -