Chiappelli F, Frost P, Manfrini E, Lee P, Pham L, Garcia C, Daley S, Kung M, Villanueva P
Laboratory of Human Oral and Molecular Immunology, Diagnostic Sciences, UCLA School of Dentistry.
Immunopharmacology. 1994 Nov-Dec;28(3):233-40. doi: 10.1016/0162-3109(94)90059-0.
Cocaine is reported to be immunotoxic. The biochemical mechanisms responsible for the immunopharmacological outcomes of cocaine in vivo and in vitro remain, however, to be fully elucidated. Our experimental data confirm that exposure of normal human T cells to micromolar concentrations of cocaine modulates T-cell responses to stimulation by a variety of stimuli, and indicate that cocaine impairs early activation events during CD4+ but not CD4- T-cell stimulation. Pre-incubation of enriched CD4+ T-cell subpopulations that express the homing receptor CD62L with nanomolar concentrations of the endogenous opioid peptide beta-endorphin leads to a more severe impairment of activation than that noted following pre-incubation with micromolar concentrations of cocaine alone. These findings begin to elucidate the molecular and cellular mechanisms of the immunopathology of cocaine. Our data support the proposition that cocaine abuse may place cocaine-abuser HIV-seropositive individuals at increased risk of opportunistic infections.
据报道，可卡因具有免疫毒性。然而，可卡因在体内和体外产生免疫药理学结果的生化机制仍有待充分阐明。我们的实验数据证实，正常人类T细胞暴露于微摩尔浓度的可卡因中会调节T细胞对多种刺激的反应，并表明可卡因会损害CD4 + T细胞刺激过程中的早期激活事件，但不会损害CD4 - T细胞刺激过程中的早期激活事件。用纳摩尔浓度的内源性阿片肽β-内啡肽对表达归巢受体CD62L的富集CD4 + T细胞亚群进行预孵育，会导致比单独用微摩尔浓度的可卡因预孵育更严重的激活损伤。这些发现开始阐明可卡因免疫病理学的分子和细胞机制。我们的数据支持这样一种观点，即可卡因滥用可能会使滥用可卡因的HIV血清阳性个体面临机会性感染的风险增加。
