Accession Number:

ADA214031

Title:

Host Defense Against Opportunist Microorganisms Following Trauma

Descriptive Note:

Annual rept.

Corporate Author:

JAMES N GAMBLE INST OF MEDICAL RESEARCH CINCINNATI OH

Personal Author(s):

Report Date:

1989-06-30

Pagination or Media Count:

42.0

Abstract:

Prostaglandins of the E series inhibit major effector functions of polymorphonuclear leukocytes PMNs by elevating intracellular cyclic-3, 5- adenosine monophosphate camp. The present study investigated the involvement of this mechanism in the bactericidal defect of PMNs induced by thermal injury in a guinea pig. Peripheral and peritoneal exudate PMNs harvested from thermally injured guinea pigs at one or two days postburn had decreased bactericidal activity against Pseudomonas aeruginosa and a marked increase in camp content. Production of prostaglandin E1 PGE1 by these cells in the absence of exogenous PMN activators was also increased. Treatment of PMNs in vitro or in vivo with nonsteroidal anti-inflammatory drugs NSAIDS indomethacin, ibuprofen, and piroxicam restored bactericidal activity to normal and concomitantly reduced camp content and PGE1 production. A concomitant reduction in camp content and PGE1 production was also observed as bactericidal activity of PMNs returned to normal under natural conditions during four to seven days postburn. The enhancement of PMN bactericidal activity mediated by NSAIDs was fully counteracted by purified PGE1, theophylline, and by camp itself. These results suggest that the bactericidal defect of PMNs induced by thermal injury is related to elevation of camp and that PGE1 plays a significant role in this phenomenon. Thermal injury Trauma Host resistance Infection Immunosuppression Polymorphonuclear leukocyte function Arachidonic acid metabolism RAII.

Subject Categories:

  • Biology
  • Medicine and Medical Research
  • Microbiology

Distribution Statement:

APPROVED FOR PUBLIC RELEASE