Journal
JOURNAL OF IMMUNOLOGY
Volume 175, Issue 10, Pages 6361-6367Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.175.10.6361
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Funding
- NIDA NIH HHS [KO2DA015349, P50DA11806, R01DA12104] Funding Source: Medline
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Impaired host defense mechanisms after major operative procedures and trauma are recognized as important factors in the development of infectious complication. Trauma is associated with impaired cellular immunity and CD4(+) T cell Th2 differentiation. We have previously implicated morphine treatment as a possible mechanism for Th2 differentiation after injury. In this investigation we first establish that morphine treatment in vivo results in Th2 differentiation and that this effect is mediated through a naltrexone-sensitive opioid receptor. We investigated the intracellular mechanism by which morphine controls CD4(+) T cell diferentiation and demonstrate that morphine treatment in vitro 1) increases anti CD3/CD28 Ab-induced CD4(+) T cell IL-4 protein synthesis, IL-4 mRNA, and GATA-3 mRNA accumulation through a pertussis toxin-sensitive receptor; 2) results in a dose-dependent increase in anti-CD3/CD28 Ab-induced CD4(+) T cell cytoplasmic cAMP concentration; and 3) increases the forskolin-stimulated cytoplasmic cAMP level through a pertussis toxin-sensitive receptor. We also demonstrate that chronic morphine treatment increases anti-CD3/CD28 Ab-induced IL-4 promoter activity and IL-4 immunoprotein expression through a p38 MAPK-dependent, but protein kinase A- and Erk1/Erk2-independent, mechanism.
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