Sacerdote P, Gaspani L, Panerai A E
Department of Pharmacology, School of Medicine, University of Milano, 20129 Milano, Italy.
Ann N Y Acad Sci. 2000;917:755-63. doi: 10.1111/j.1749-6632.2000.tb05440.x.
Opioid peptides affect different immune functions. We present evidence that these effects could be mediated by the modulation of Th1/Th2 cytokine production. The acute and chronic treatment with the opioid receptor antagonist naloxone decreased the production of IL-4 by splenocytes of C57BL/6 and Balb/cJ mice, that present a Th1/Th2 dominance, respectively, immunized with the protein antigen KLH. In contrast, IL-2 and IFN-gamma levels were increased after naloxone treatment. These results indicate that naloxone increases Th1 and decreases Th2 cytokine production. Moreover in C57BL/6 mice, naloxone treatment was able to accelerate skin-graft rejection, a Th1-mediated phenomenon, by increasing Th1 cytokine production. The effect of naloxone could be ascribed to the removal of the regulatory effects exerted by endogenous opioid peptides, which could activate Th2 and suppress Th1 cytokines.
阿片肽会影响不同的免疫功能。我们提供的证据表明，这些效应可能是通过调节Th1/Th2细胞因子的产生来介导的。用阿片受体拮抗剂纳洛酮进行急性和慢性处理，可降低分别以Th1/Th2为主导的C57BL/6和Balb/cJ小鼠脾细胞中IL-4的产生，这些小鼠用蛋白抗原钥孔戚血蓝蛋白（KLH）免疫。相反，纳洛酮处理后IL-2和干扰素-γ水平升高。这些结果表明，纳洛酮可增加Th1细胞因子的产生并减少Th2细胞因子的产生。此外，在C57BL/6小鼠中，纳洛酮处理能够通过增加Th1细胞因子的产生来加速皮肤移植排斥反应，这是一种由Th1介导的现象。纳洛酮的作用可能归因于去除了内源性阿片肽所发挥的调节作用，内源性阿片肽可激活Th2细胞因子并抑制Th1细胞因子。
