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(Journal of Leukocyte Biology. 2000;68:821-827.)
© 2000 by Society for Leukocyte Biology

Neutrophil migration stimulates rat intestinal epithelial cell cytokine expression during helminth infection

Andrew W. Stadnyk*, Cheryl D. Dollard* and Andrew C. Issekutz*,{dagger},{ddagger}

* Departments of Pediatrics,
{dagger} Microbiology and Immunology, and
{ddagger} Pathology, Dalhousie University, and the Dalhousie Inflammation Group, Halifax, Nova Scotia, Canada

Correspondence: Andrew Stadnyk, Ph.D., Infection and Immunology Research Laboratories, IWK Grace Health Centre, 5850 University Avenue, Halifax, Nova Scotia, B3J 3G9 Canada. E-mail: Andrew.Stadnyk{at}Dal.Ca

We are interested in understanding the role of epithelial cells during inflammation, and we previously reported that rat small intestinal epithelial cells express interleukin-1ß (IL-1ß) during infection by Trichinella spiralis. We now report that the epithelium also produces the potent neutrophil chemotactic factor, macrophage inflammatory protein-2 (MIP-2), and an IL-1 antagonist: the type II IL-1 receptor. Consequently we investigated the pattern of neutrophil infiltration into the infected intestine, which closely paralleled the epithelial cytokine expression. Speculating that neutrophil infiltration may provoke epithelial cytokine expression, neutrophil migration into the infected gut was reduced by depleting circulating cells through the use of a specific antibody, or by preventing migration through the use of a function-blocking anti-CD18 monoclonal antibody. Either treatment reduced the number of neutrophils recoverable from the small intestinal epithelium and was paralleled by reduced mRNA levels for epithelial cytokines. These results demonstrate that neutrophil infiltration of the small intestinal epithelium contributes to the stimulation of epithelial cell cytokines.

Key Words: Trichinella spiralis • interleukin-1 • macrophage inflammatory peptide-2




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