在2008年4月15日出版《BMC細(xì)胞生物學(xué)》（BMC Cell Biology）上的最新研究顯示,，尼古丁會(huì)降低嗜中性粒細(xì)胞尋找并消滅細(xì)菌的能力，而這種存活時(shí)間很短的白血細(xì)胞能夠有效地抗感染,。
嗜中性粒細(xì)胞是由人的骨髓產(chǎn)生的，經(jīng)過(guò)一定時(shí)期會(huì)轉(zhuǎn)變?yōu)槠渌募?xì)胞,。盡管尼古丁影響嗜中性粒細(xì)胞是眾所周知的,，但是直到現(xiàn)在科學(xué)家們才對(duì)尼古丁在嗜中性粒細(xì)胞轉(zhuǎn)化過(guò)程中的作用機(jī)理有研究。
作者表明他們所觀察到的過(guò)程損害了嗜中性粒細(xì)胞,，這部分解釋了長(zhǎng)期吸煙者會(huì)增加細(xì)菌感染和炎癥疾病的幾率,。（來(lái)源：科學(xué)報(bào)道沙龍）
生物谷推薦原始出處：
（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.
