Brett Kyle, Parker Renée, Wittenauer Shannon, Hayashida Ken-Ichiro, Young Tracey, Vincler Michelle
Department of Anesthesiology, and Center for the Study of Pharmacological Plasticity in the Presence of Pain, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
J Neuroimmunol. 2007 May;186(1-2):37-44. doi: 10.1016/j.jneuroim.2007.02.005. Epub 2007 Mar 23.
Chronic nicotine exposure and the immune response to peripheral nerve injury has not been investigated thoroughly. Rats were exposed to chronic nicotine or saline followed by chronic constriction injury (CCI) of the sciatic nerve. Mechanical sensitivity was measured at various time points and the immune response was investigated at 21 days post-CCI. Chronic nicotine increased mechanical hypersensitivity, microglia activation, and the production of IL-1beta, but not the number of immune cells at the site of injury. These results suggest that chronic nicotine increases mechanical hypersensitivity following peripheral nerve injury through a mechanism that may involve an increased production and release of central and peripheral cytokines.
慢性尼古丁暴露与对周围神经损伤的免疫反应尚未得到充分研究。将大鼠暴露于慢性尼古丁或生理盐水中,随后对坐骨神经进行慢性压迫损伤(CCI)。在不同时间点测量机械敏感性,并在CCI后21天研究免疫反应。慢性尼古丁增加了机械超敏反应、小胶质细胞活化和IL-1β的产生,但没有增加损伤部位的免疫细胞数量。这些结果表明,慢性尼古丁通过一种可能涉及增加中枢和外周细胞因子产生和释放的机制,增加周围神经损伤后的机械超敏反应。