Down-Regulation of Chemotaxis of Polymorphonuclear Leukocytes following Thermal Injury Involves Two Distinct Mechanisms

Thermal injury induces a depression of major effector functions of polymorphonuclear leukocytes (PMNL) that contributes to the increased susceptibility to bacterial infection associated with severe injury. In a study on chemotactic alterations in PMNL induced by thermal injury in a well-characterize...

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Bibliographic Details
Published in:The Journal of infectious diseases 1993-07, Vol.168 (1), p.120-127
Main Authors: Bjornson, Ann B., Somers, Scott D.
Format: Article
Language:English
Subjects:
Actins
Analysis of Variance
Animal migration behavior
Animals
Anti-Inflammatory Agents, Non-Steroidal - pharmacology
Burns - immunology
Cells, Cultured
Chemotactic factors
Chemotaxis
Chemotaxis, Leukocyte
Cyclic AMP - metabolism
Down regulation
Female
Formyl peptide receptors
Guinea Pigs
Leukocytes
Major Articles
Male
N-Formylmethionine Leucyl-Phenylalanine - pharmacology
Neutrophils
Neutrophils - immunology
Physical trauma
Receptors
Receptors, Formyl Peptide
Receptors, Immunologic - metabolism
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Summary:Thermal injury induces a depression of major effector functions of polymorphonuclear leukocytes (PMNL) that contributes to the increased susceptibility to bacterial infection associated with severe injury. In a study on chemotactic alterations in PMNL induced by thermal injury in a well-characterized guinea pig model, a concomitant reduction in the chemotactic response of PMNL to zymosan-activated serum (ZAS) and FMLP was seen early after thermal injury in temporal association with the previously reported bactericidal defect and depression of superoxide anion production. Unlike the bactericidal defect, the chemotactic alterations were not directly linked to the marked elevation of intracellular cAMP in PMNL associated with thermal injury. Two mechanisms (adaptation and desensitization) were shown to be involved in the reduction of chemotactic responses of PMNL to FMLP and ZAS, respectively. Adaptation appears to be a protective response of PMNL to thermal injury unassociated with receptor down-regulation.
ISSN:0022-1899
1537-6613
DOI:10.1093/infdis/168.1.120