Sopori M L, Kozak W, Savage S M, Geng Y, Kluger M J
Pathophysiology Division, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA.
Adv Exp Med Biol. 1998;437:279-89. doi: 10.1007/978-1-4615-5347-2_31.
Tobacco smoking may predispose humans to respiratory disease, and may be a compounding risk factor in HIV infection and progression to AIDS. We have demonstrated that chronic exposure of mice and rats to cigarette smoke or nicotine inhibits T cell responsiveness, which may account for the decreased antibody response to T-dependent antigens seen in these animals. This inhibition may result from aberrant antigen-mediated signaling and depletion of IP3-sensitive Ca2+ stores in nicotine-treated animals. Moreover, nicotine appears to moderate the inflammation associated with turpentine-induced sterile abscess and influenza infection. These anti-inflammatory properties of nicotine may account for longer survival of nicotine-treated than control mice lethally infected with influenza virus. However, because inflammation is required for clearance of many pathogens, nicotine-treated mice exhibit significantly higher titers of influenza virus following infection. These results offer an explanation for the higher susceptibility to some infectious diseases, but greater resistance to some inflammatory diseases among human smokers.
吸烟可能使人类易患呼吸道疾病，并且可能是HIV感染及发展为艾滋病的一个复合风险因素。我们已经证明，小鼠和大鼠长期暴露于香烟烟雾或尼古丁会抑制T细胞反应性，这可能解释了在这些动物中观察到的对T细胞依赖性抗原的抗体反应降低。这种抑制可能是由于抗原介导的信号异常以及尼古丁处理的动物中IP3敏感的Ca2+储存耗竭所致。此外，尼古丁似乎能减轻与松节油诱导的无菌脓肿和流感感染相关的炎症。尼古丁的这些抗炎特性可能解释了经尼古丁处理的小鼠比感染致死剂量流感病毒的对照小鼠存活时间更长的原因。然而，由于清除许多病原体需要炎症反应，感染后经尼古丁处理的小鼠流感病毒滴度显著更高。这些结果为人类吸烟者对某些传染病易感性更高，但对某些炎症性疾病抵抗力更强提供了解释。
