Chronic nicotine inhibits inflammation and promotes influenza infection
Chronic nicotine inhibits inflammation and promotes influenza infection
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DOI：
10.1016/j.cellimm.2004.07.007
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发表时间：
2004-07-01
影响因子：
4.3
通讯作者：
Sopori, ML
中科院分区：
文献类型：
--
作者：
Razani-Boroujerdi, S;Singh, SP;Sopori, ML
流行病学数据表明吸烟、呼吸道感染和伤口愈合受损之间存在关联。炎症对于人体防御病原体和伤口愈合过程至关重要。尽管尼古丁用于治疗一些炎症性疾病，但其作用机制在很大程度上尚不清楚。为了确定尼古丁如何影响炎症，通过微渗泵将大鼠和小鼠暴露于尼古丁，并评估对松节油或流感病毒的炎症反应。结果显示，虽然尼古丁抑制白细胞向炎症/感染部位迁移，但它增加了肺部的流感滴度。炎症的减少与外周血单核细胞 (PBMC) 对甲酰基-甲硫氨酰-亮氨酰-苯丙氨酸和单核细胞趋化蛋白-1 的趋化性/趋化作用降低相关，而不影响其各自受体的密度。然而，尼古丁抑制了 PBMC 中趋化因子诱导的 Ca2+ 反应，表明趋化因子信号传导受损。因此，由于尼古丁抑制白细胞迁移，因此可能会导致吸烟者伤口愈合延迟和呼吸道感染发生率增加。 (C) 2004 Elsevier Inc. 保留所有权利。
Epidemiological data suggest an association between smoking, respiratory infections, and impaired wound healing. Inflammation is critical in the body's defense against pathogens and in the wound-healing process. Although nicotine is used to treat some inflammatory conditions, the mechanism of this action is largely unknown. To determine how nicotine affects inflammation, rats and mice were exposed to nicotine via miniosmotic pumps, and the inflammatory response to turpentine or influenza virus was assessed. Results showed that while nicotine suppressed the migration of leukocytes to the inflammation/infection site, it increased the influenza titer in the lung. The decreased inflammation correlated with lower chemotaxis/chemokinesis of peripheral blood mononuclear cells (PBMC) toward formyl-methionyl-leucyl-phenylalanine and monocyte chemoattractant protein-1 without affecting the density of their respective receptors. However, nicotine suppressed the chemokine-induced Ca2+ response in PBMC, indicating impaired chemokine signaling. Thus, because nicotine suppresses leukocyte migration, it might contribute to the delayed wound healing and increased incidence of respiratory infections among smokers. (C) 2004 Elsevier Inc. All rights reserved.