Cigarette smoke exposure markedly compromises the ability of the immune system to protect against invading pathogens and tumorigenesis. Nicotine is a psychoactive component of tobacco products that acts as does the natural neurotransmitter, acetylcholine, on nicotinic receptors (nAChRs). Here we demonstrate that natural killer (NK) cells strongly express nAChR Î²2. Nicotine exposure impairs the ability of NK cells to kill target cells and release cytokines, a process that is largely abrogated by nAChR Î²2 deficiency. Further, nicotinic suppression of NF-ÎºB-induced transcriptional activity in NK cells is dependent on nAChR Î²2. This nAChR subtype also plays a large role in the NK cell-mediated control of melanoma lung metastasis, in a murine lung metastasis model exposed to nicotine. Our findings suggest nAChR Î²2 as a prominent pathway for nicotine induced impairment of NK cell functions which contributes to the occurrence of smoking-related pathologies. Â© 2013 Hao et al.
Digital Object Identifier (DOI)
Hao, Junwei; Shi, Fu Dong; Abdelwahab, Mohammed; Shi, Samuel X.; Simard, Alain; Whiteaker, Paul; Lukas, Ronald; and Zhou, Qinghua, "Nicotinic Receptor Î²2 Determines Nk Cell-Dependent Metastasis In A Murine Model Of Metastatic Lung Cancer" (2013). Neurobiology. 262.