Signaling mechanisms of elevated neutrophil Og generation after burn injury

Farideh Sabeh*, Philip E Hockberger, Mohammed M. Sayeed

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

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 C2- generation was ascertained by evaluating the effect of treatment of the rats with the Ca2+ entry blocker, diltiazem. There was an overt enhancement of O2- generation by polymorphonuclear leukocytes from burn rats on days 1, 3, and 7 postburn, with the peak release occurring on day 3 postburn. O2- generation comparable to the sham was noted on day 10 after the burn. O2- releases on days 1,3, and 7 postburn were accompanied by marked elevation of Cai2+ and PKC responses. Like the O2- 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 O2- 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 O2- generation and degranulation, our results suggest that neutrophil O2- release enhancement in the early stages after burn injury (e.g., days 1-7 postburn) results from an overactivation of the Cai2+ and PKC signaling pathways. The heightened O2- generation during the early burn injury phase might play a role in tissue damage in one or more of host organs.

Original languageEnglish (US)
JournalAmerican Journal of Physiology
Volume274
Issue number2 PART 2
StatePublished - Dec 1 1998

Keywords

  • Intracellular calcium antagonist
  • Intracellular calcium signaling
  • Protein kinase c activation
  • Rat
  • Reduced nicotinamide adenine dinucleotide phosphate oxidase
  • Thermal injury

ASJC Scopus subject areas

  • Physiology (medical)

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