@article{oai:kobe-c.repo.nii.ac.jp:00001896,
 author = {平林, 玲子 and 西田, 昌司 and HIRABAYASHI, Reiko and NISHIDA, Masashi},
 issue = {1},
 journal = {神戸女学院大学論集, KOBE COLLEGE STUDIES},
 month = {Jun},
 note = {P(論文), Cigarette smoke contains more than 4,000 chemical substances and causes deleterious effects on various human organs. As the lung is the first organ that is exposed to these substances, cigarette smoking induces respiratory diseases such as inflammation, remodeling and cancer in high incidence. We examined whether nicotine, one of the major bioactive substances in cigarette smoke, disrupts lung immune function against respiratory diseases. We tested the effect of nicotine on antimicrobial activity of alveolar macrophages (AMs) by evaluating nitric oxide (NO) production and phagocytosis. NO production was assessed by measuring N0_2^-/N0_3^-concentration using Griess reagent method and phagocytosis was evaluated by the intake of fluoroprobe-labeled latex beads. Rat AM harvested by blonchoalveolar lavage (BAL) and mouse AM cell line (AMJ2-C11) were treated with 0-500μM of nicotine for 24h. Nicotine in high concentration (250, 500μM) enhanced phagocytosis of latex beads in both AMs significantly. In addition, the high concentration of nicotine (over 100μM) increased NO production by AMs. These results suggeste that nicotine enhances inflammatory function of AMs in high concentration. The over activation of inflammatory response by nicotine may contribute to the induction of respiratory injury by cigarette smoking.},
 pages = {105--117},
 title = {肺胞マクロファージの炎症反応に及ぼすニコチンの影響},
 volume = {55},
 year = {2008},
 yomi = {ヒラバヤシ, レイコ and ニシダ, マサシ}
}