Background: Cigarette smoke (CS) is inhaled into the lung. Alveolar macrophage (AM)
is known to play an important role in the lung immune system. However, the relationship between
AM functions and antibody production by CS is not fully investigated.
Objective: Therefore, we investigated the effects of AM from CS exposed mice on antibody production.
Mice were exposed to 20 cigarettes/day for 10 days. AM were obtained by broncho-alveolar
lavage. Antibody production was analyzed by plaque-forming cell assay using seep red blood
cell (SRBC) as antigen.
Methods: B cell proliferation was analyzed by 3H-thymidine incorporation. Phagocytic activity using
fluorescein isothiocyanate-labeled SRBC and expressions of surface antigens on AM were analyzed
by flow cytometry. Cytokines and NF-κB mRNA expressions of AM were analyzed by RTPCR.
Results and Discussion: Antibody production was decreased at the induction phase, but not at the
expression phase by AM from smoked mice (SM) compared with non-smoked mice (NSM). B cell
proliferation was decreased by cigarette extracts dose-dependently. Phagocytic activity of AM was
decreased in SM compared with NSM. Expression of surface antigens on AM was decreased in
SM compared with NSM. Cytokines or NF-κB mRNA expressions of AM were decreased in SM
compared with NSM.
Conclusion: These results suggest that the inhibition of antibody production by cigarette smoking
is caused by the inhibition of phagocytosis and expressions of surface antigens associated with antigen
presentation. Such inhibition of AM functions may increase the risk of bacterial and virus infections.