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(Journal of Leukocyte Biology. 2000;68:251-259.)
© 2000 by Society for Leukocyte Biology

Parallel induction of epithelial surface-associated chemokine and proteoglycan by cellular hypoxia: implications for neutrophil activation

Glenn T. Furuta^*,, Andrea L. Dzus^*, Cormac T. Taylor^* and Sean P. Colgan^*

^* Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women’s Hospital; and
Combined Program in Pediatric Gastroenterology and Nutrition, Children’s Hospital, and Harvard Medical School, Boston, Massachusetts

Correspondence: Sean P. Colgan, Ph.D., Brigham and Women’s Hospital, Center for Experimental Therapeutics and Reperfusion Injury, Thorn 704, 75 Francis Street, Boston, MA 02115. E-mail: colgan{at}zeus.bwh.harvard.edu

Neutrophil-induced damage to the protective epithelium has been implicated in mucosal disorders associated with hypoxia, and such damage may be initiated by epithelial-derived chemokines. Because chemokines can bind to membrane proteoglycans, we hypothesized that chemokines may associate with epithelial surfaces and activate polymorphonuclear neutrophils (PMN). Epithelial hypoxia (pO₂ 20 torr) resulted in a time-dependent induction of interleukin-8 (IL-8) mRNA, soluble protein, as well as surface protein. Such surface IL-8 expression was demonstrated to be dependent on heparinase III expression, and extensions of these experiments indicated that hypoxia induces epithelial perlecan expression in parallel with IL-8. Finally, co-incubation of post-hypoxic epithelia with human PMN induced IL-8-dependent expression of the PMN ß₂-integrin CD11b/18. These data indicate that chemokines liberated from epithelia may exist in a surface-bound, bioactive form and that hypoxia may regulate proteoglycan expression.

Key Words: interleukin-8 • mucosal disorders • hypoxia

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