在2008年4月15日出版《BMC细胞生物学》（BMC Cell Biology）上的最新研究显示，尼古丁会降低嗜中性粒细胞寻找并消灭细菌的能力，而这种存活时间很短的白血细胞能够有效地抗感染。
嗜中性粒细胞是由人的骨髓产生的，经过一定时期会转变为其他的细胞。尽管尼古丁影响嗜中性粒细胞是众所周知的，但是直到现在科学家们才对尼古丁在嗜中性粒细胞转化过程中的作用机理有研究。
作者表明他们所观察到的过程损害了嗜中性粒细胞，这部分解释了长期吸烟者会增加细菌感染和炎症疾病的几率。（来源：科学报道沙龙）
生物谷推荐原始出处：
（BMC Cell Biology），doi:10.1186/1471-2121-9-19，Minqi Xu , David A Scott
The influence of nicotine on granulocytic differentiation - inhibition of the oxidative burst and bacterial killing and increased matrix metalloproteinase-9 release
Minqi Xu , James E Scott , Kan-Zhi Liu , Hannah R Bishop , Diane E Renaud , Richard M Palmer , Abdelilah Soussi-Gounni and David A Scott
Background
Neutrophils leave the bone marrow as terminally differentiated cells, yet little is known of the influence of nicotine or other tobacco smoke components on neutrophil differentiation. Therefore, promyelocytic HL-60 cells were differentiated into neutrophils using dimethylsulfoxide in the presence and absence of nicotine (3-(1-methyl-2-pyrrolidinyl) pyridine). Differentiation was evaluated over 5 days by monitoring terminal differentiation markers (CD11b expression and formazan deposition); cell viability, growth phase, kinetics, and apoptosis; assessing cellular morphology and ultrastructure; and conformational changes to major cellular components. Key neutrophil effector functions (oxidative burst, bacterial killing, matrix metalloproteinase release) were also examined. Results: Nicotine increased the percentage of cells in late differentiation phases (metamyelocytes, banded neutrophils and segmented neutrophils) compared to DMSO alone (p < 0.05), but did not affect any other marker of neutrophil differentiation examined. However, nicotine exposure during differentiation suppressed the oxidative burst in HL-60 cells (p < 0.001); inhibited bacterial killing (p < 0.01); and increased the LPS-induced release of MMP-9, but not MMP-2 (p < 0.05). These phenomena may be alpha-7-acetylcholine nicotinic receptor-dependent. Furthermore, smokers exhibited an increased MMP-9 burden compared to non-smokers in vivo (p < 0.05). Conclusions: These findings may partially explain the known increase in susceptibility to bacterial infection and neutrophil-associated destructive inflammatory diseases in individuals chronically exposed to nicotine.
