Abstract
Abstract Morphine is a widely-used drug for analgesics and drug abuse. Previous studies have also demonstrated that the widely used as an anesthetic agent as well as adjuvant for the treatment of cancer pain and neuropathic pain, will bring harmful effects on specific immune system. Furthermore, the suppressed immune function may lead to postoperative infection and postoperative dissemination of carcinoma. Our research team has confirmed that morphine could promote tumor growth in naïve immunocompromised mice in our previous project, and morphine could suppress the proliferative ability of T lymphocytes even erased the tumor protection effects enhanced by tumor vaccines in vivo. However, these apoptotic phenomena could not explain the complete reasons that morphine induced tumor progression. The antigen processing and presenting activity enhanced by antigen presenting cells is the main cause in tumor development, especially in dendritic cells. The tumorgenesis is always associated with the low antigen presentation activity, and it results the poor recognization by cytotoxic T cells even causes the immuno-escape responses. In the present study, we confirmed that the efficiency of bone marrow monocytes differentiate into dendritic cells was significantly decreased after morphine stimulation. Under high dose morphine treatment, more than 30 % of differentiation efficiency was eliminated in 6 days incubation. Besides, the expression of co-stimulation factor CD80 and CD86 were both decrease after morphine treatment. Furthermore, cytokine expression including IL-6 and TNF-α were both inhibited, however, only IL-10 was slightly increase after morphine stimulation. Besides, the antigen processing and presenting activity of ex-vivo bone marrow-derived dendritic cells were reduced after morphine stimulation. These results suggested that morphine might reduce the process of dendritic cells maturation. These results provided the complete molecular mechanism and the correlation between morphine and immunity. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5401. doi:1538-7445.AM2012-5401
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