Neutrophil Transepithelial Migration and Epithelial Barrier Function in IBD

Potential Targets for Inhibiting Neutrophil Trafficking

  1. ALEX C. CHIN,
  2. CHARLES A. PARKOS

Article first published online: 24 AUG 2006

DOI: 10.1196/annals.1326.018

Issue

Annals of the New York Academy of Sciences

Additional Information

How to Cite

CHIN, A. C. and PARKOS, C. A. (2006), Neutrophil Transepithelial Migration and Epithelial Barrier Function in IBD. Annals of the New York Academy of Sciences, 1072: 276–287. doi: 10.1196/annals.1326.018

Author Information

  1. Epithelial Pathobiology Unit, Department of Pathology and Laboratory Medicine, Emory University Atlanta, Georgia 30322, USA

*Address for correspondence: Charles A. Parkos, M.D., Ph.D., Department of Pathology and Laboratory Medicine, Emory University, 615 Michael Street, Atlanta, GA, USA 30322. Voice: 404-727-8533; fax: 404-727-8538.  e-mail: cparkos@emory.edu

Publication History

  1. Issue published online: 24 AUG 2006
  2. Article first published online: 24 AUG 2006

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Keywords:

  • meutrophil;
  • transmigration;
  • epithelium;
  • apical junction complex;
  • permeability;
  • IBD

Abstract: Neutrophil (PMN) transmigration across mucosal epithelia is a hallmark of inflammatory conditions, such as ulcerative colitis and Crohn's disease. PMN accumulation within epithelial crypts and in the intestinal lumen directly correlates with clinical disease activity and epithelial injury. Currently, the mechanisms by which PMNs migrate across mucosal epithelia are incompletely understood and a better understanding of this process will likely provide new insights into novel treatment strategies for inflammatory bowel disease. In this article, we discuss current advances that define PMN transepithelial migration, specifically focusing on PMN–epithelial adhesive interactions and signaling events. We also describe how these interactions might be specifically targeted for the development of therapeutic strategies to manage mucosal inflammation.

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