Host Defense against Opportunist Microorganisms Following Trauma
Abstract
The purpose of this study was to determine the involvement of cyclooxygenase and lipoxygenase metabolites in the depression of host defense induced by thermal injury in a guinea pig model. We found that the bactericidal defect of neutrophils induced by thermal injury in this model was related to a marked elevation of intracellular cyclic-3',5'- adenosine monosphate (cAMP), which in turn was related to autogenous prostaglandin (PG) El production by these cells. Suppression of PGE1 production by in vivo or in vitro treatment of neutrophils with selective cyclooxygenase inhibitors normalized intracellular CAMP and correct the bactericidal defect. Despite the profound effects of cyclooxygenase inhibitors on neutrophil function, these drugs were not found to influence the depression of cell-mediated immune responses induced by thermal injury in guinea pig or mouse models. These drugs also had no effect on survival or the time to death following experimental burn wound sepsis with Pseudomonas aeruginosa or Proteus mirabilis. No evidence was obtained supporting involvement of lipoxygenase metabolites in the bactericidal defect of neutrophils or the depression of cell-mediated immune responses induced by thermal injury. In summary, our study has pinpointed the mechanism responsible for the bactericidal defect of neutrophils in a guinea pig model of thermal injury. In addition, our results ruled out a major role for cyclooxygenase or lipoxygenase metabolites in mediating the depression of cell-mediated immune responses following thermal injury in several animal models.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 30, 1991
- Accession Number
- ADA249998
Entities
People
- Ann B. Bjornson
- H. S. Bjornson