Department of Microbiology, Molecular Genetics, and Immunology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Br J Pharmacol. 2011 Dec;164(7):1829-44. doi: 10.1111/j.1476-5381.2011.01475.x.
Opioid use and abuse has been linked to significant immunosuppression, which has been attributed, in part, to drug-induced depletion of lymphocytes. We sought to define the mechanisms by which lymphocyte populations are depleted and recover following morphine treatment in mice.
Mice were implanted with morphine pellets and B- and T-cell subsets in the bone marrow, thymus, spleen and lymph nodes were analysed at various time points. We also examined the effects of morphine on T-cell development using an ex vivo assay.
The lymphocyte populations most susceptible to morphine-induced depletion were the precursor cells undergoing selection. As the lymphocytes recovered, more lymphocyte precursors proliferated than in control mice. In addition, peripheral T-cells displayed evidence that they had undergone homeostatic proliferation during the recovery phase of the experiments.
The recovery of lymphocytes following morphine-induced depletion occurred in the presence of morphine and via increased proliferation of lymphoid precursors and homeostatic proliferation of T-cells.
阿片类药物的使用与滥用与显著的免疫抑制有关,部分原因是药物诱导的淋巴细胞耗竭。我们试图确定吗啡治疗后小鼠淋巴细胞群耗竭和恢复的机制。
将吗啡丸植入小鼠体内,并在不同时间点分析骨髓、胸腺、脾脏和淋巴结中的 B 细胞和 T 细胞亚群。我们还使用体外测定法研究了吗啡对 T 细胞发育的影响。
最易受吗啡诱导耗竭影响的淋巴细胞群是正在进行选择的前体细胞。随着淋巴细胞的恢复,增殖的淋巴细胞前体比对照组小鼠更多。此外,外周 T 细胞显示出在实验恢复阶段经历了稳态增殖的证据。
吗啡诱导耗竭后淋巴细胞的恢复是在存在吗啡的情况下通过增加淋巴细胞前体的增殖和 T 细胞的稳态增殖来实现的。