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Am J Physiol Regul Integr Comp Physiol 274: R476-R485, 1998;
0363-6119/98 $5.00
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Vol. 274, Issue 2, R476-R485, February 1998

Signaling mechanisms of elevated neutrophil O<SUP>−</SUP><SUB>2</SUB> generation after burn injury

Farideh Sabeh1,2, Philip Hockberger3, and Mohammed M. Sayeed1,2,4

Departments of 1 Physiology and 4 Surgery and 2 Burn and Shock Trauma Institute, Stritch School of Medicine, Loyola University of Chicago, Maywood 60153; and 3 Department of Physiology, Northwestern University Medical School, Chicago, Illinois 60611

A full skin thickness burn injury was produced in anesthetized rats by exposing 25% of total body surface area to 98°C water for 10 s. Sham (exposed to 37°C water) and burn rats were killed 1, 3, 7, or 10 days later. The role of Ca2+ signaling and Ca2+-related protein kinase C (PKC) activation in neutrophil O<SUP>−</SUP><SUB>2</SUB> generation was ascertained by evaluating the effect of treatment of the rats with the Ca2+ entry blocker, diltiazem. There was an overt enhancement of O<SUP>−</SUP><SUB>2</SUB> generation by polymorphonuclear leukocytes from burn rats on days 1, 3, and 7 postburn, with the peak release occurring on day 3 postburn. O<SUP>−</SUP><SUB>2</SUB> generation comparable to the sham was noted on day 10 after the burn. O<SUP>−</SUP><SUB>2</SUB> releases on days 1, 3, and 7 postburn were accompanied by marked elevation of Ca2+i and PKC responses. Like the O<SUP>−</SUP><SUB>2</SUB> release, intracellular Ca2+ concentration ([Ca2+]i) response on day 10 after burn was suppressed to levels found in the sham group. The treatment of burn rats with diltiazem prevented the upregulation of both [Ca2+]i and PKC responses as well as O<SUP>−</SUP><SUB>2</SUB> generation in neutrophils in rats on days 1, 3, and 7 after the burn. Because previous studies have shown that increases in [Ca2+]i precede O<SUP>−</SUP><SUB>2</SUB> generation and degranulation, our results suggest that neutrophil O<SUP>−</SUP><SUB>2</SUB> release enhancement in the early stages after burn injury (e.g., days 1-7 postburn) results from an overactivation of the Ca2+i and PKC signaling pathways. The heightened O<SUP>−</SUP><SUB>2</SUB> generation during the early burn injury phase might play a role in tissue damage in one or more of host organs.

thermal injury; rat; intracellular calcium signaling; protein kinase C activation; reduced nicotinamide adenine dinucleotide phosphate oxidase; intracellular calcium antagonist


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