Tobacco smoking is a significant risk factor in respiratory diseases including chronic obstructive lung disease and pneumonia.The bronchial alveolar lavage fluids obtained from tobacco smokers have increased number of alveolar macrophages and neutrophils.(1,2) Moreover, compared with nonsmokers, alveolar macrophages from smokers appear to be in an active state, exhibiting increased microsomal and lysosomal enzymes, elevated resting rates of glucose use, increased production of oxygen radicals and myeloperoxidase activity, and increased migration and chemotactic responsiveness.(3) However, despite this increased activity, alveolar macrophages from smokers appear to be deficient in phagocytosis and bactericidal activity.(4) Therefore, it has been conjectured that tobacco smoking may cause a disruption of normal lung immune function against respiratory infections. In fact, it is widely accepted that tobacco smoking is one of the risk factors for respiratory infections.5–7 For instance, pneumonia caused by Streptococcus pneumoniae, the most common causative bacteria of community-acquired pneumonia, is accelerated by smoking.(8) Pneumonia caused by other bacteria, such as Legionella and Chlamydia, also frequently occurs in smokers.5–7 However, little is known about the effect of tobacco components on antimicrobial activity and immune responses of alveolar macrophages. Nicotine, a small organic alkaloid synthesized by tobacco plants, is the addictive component of tobacco.This small alkaloid acts as an agonist at the nicotinic