Background::
Cigarette smoke (CS) is inhaled into lung. Alveolar macrophage (AM) is known to play an
important role in lung immune system. However, the relationship of 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 during 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 RT-PCR.
Results and Discussion:
Antibody production was decreased at induction phase, but not expression phase by AM from
smoked mice (SM) compared with non-smoked mice (NSM). B cell proliferation was decreased by cigarette extracts at
dose dependent. Phagocytic activity of AM was decreased in SM compared with NSM. Expression of surface antigens on
AM were 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 be increased the risk of bacterial and virus infections.
IRF-2 regulates B-cell proliferation and antibody production through distinct mechanisms