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This Article Full Text (PDF) All Versions of this Article: jas.2008-1339v1 87/14_suppl/E101    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Lambert, G. P. Search for Related Content PubMed PubMed Citation Articles by Lambert, G. P.

Stress-induced gastrointestinal barrier dysfunction and its inflammatory effects

Department of Exercise Science, Creighton University, Omaha, NE 68178

plambert{at}creighton.edu

Abstract

The intestinal barrier is formed by enterocyte membranes, tight junctions, secreted mucus, and immunologic factors, such as tissue macrophages. Dysfunction of this barrier can be caused by different types of stress (e.g., physiological, pathological, psychological, pharmacological) and can lead to increased intestinal permeability. Increased permeability to endotoxin, a component of the walls of Gram-negative bacteria, causes local and(or) systemic inflammatory reactions. The immune response(s) can then promote more serious conditions. Exertional heat stroke is an example of such a condition. During severe exercise-heat stress, possibly combined with other stresses, reductions in intestinal blood flow and(or) direct thermal damage to the intestinal mucosa can cause intestinal barrier disruption and endotoxemia. The resulting inflammatory response is believed to be involved in altered thermoregulation and multiple-organ dysfunction. Possible means for preventing and(or) attenuating many stress-induced intestinal barrier problems include environmental, pharmaceutical, and(or) nutritional approaches.

Key Words: endotoxin • heat • inflammation • intestine • nutrition • stress