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Department of Medical Microbiology and Immunology, University of South Florida College of Medicine, Tampa, FL 33612
Although nicotine is thought to be one of the major
immunomodulatory components of cigarette smoking, how nicotine alters
the host defense of the lung and, in particular, immune responses of
alveolar macrophages, which are critical effector cells in the lung
defense to infection, is poorly understood. Nicotinic acetylcholine
receptors (nAChRs) are the receptor for nicotine and may be involved in
the modulation of macrophage function by nicotine. In this study,
therefore, nicotine-induced suppression of antimicrobial activity and
cytokine responses of alveolar macrophages mediated by nAChRs to
Legionella pneumophila, a causative agent for pneumonia,
were examined. The murine MH-S alveolar macrophage cell line cells
expressed the messages for 
4 and 
2 subunits of nAChRs, but not
7 subunits, determined by RT-PCR. The nicotine treatment of MH-S
alveolar macrophages after infection with L. pneumophila
significantly enhanced the replication of bacteria in the macrophages
and selectively down-regulated the production of IL-6, IL-12, and
TNF-, but not IL-10, induced by infection. These effects were
completely blocked by a nonselective antagonist,
d-tubocurarine, for nAChRs, but not by a selective
antagonist, -bungarotoxin, for 7-nAChRs. Furthermore, the
stimulation of nAChRs with another agonist,
1,1-dimethyl-4-phenylpiperazinium iodide, showed the same effects,
which were blocked by the antagonist d-tubocurarine, on
the bacterial replication and cytokine regulation with that of
nicotine. Thus, the results revealed that nAChRs, the major exogenous
ligands of which are nicotine, are involved in the regulation of
macrophage immune function by nicotine and may contribute to the
cigarette-induced risk factors for respiratory infections in
smokers.
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