Alveolar macrophage from cigarette smoke-exposed mice inhibits B lymphocyte proliferation stimulated with LPS.

ABSTRACT

BACKGROUND: Smokers have higher incidences of pulmonary diseases. This increased susceptibility may result from cigarette smoke (CS)-induced impairment of the pulmonary immune system. However, the mechanism(s) is not fully understood. OBJECTIVE: The aim of this study was to investigate the mechanism of the effect of alveolar macrophages (AM) from CS-exposed mice on B lymphocyte proliferation stimulated with bacterial lipopolysaccharide (LPS). METHODS: Mice were exposed to CS using a Hamburg smoking machine, and AM were obtained by bronchoalveolar lavage. Lymphocytes were harvested from spleen in normal mice. AM-mediated B lymphocyte proliferation stimulated with LPS was assessed by the (3)H-thymidine method, using lymphocytes as responding cells and AM from CS-exposed or non-CS-exposed mice. Generations of superoxide and hydrogen peroxide were analyzed by flow cytometry, using hydroethidine and dichlorofluorescein diacetate. RESULTS: AM from CS-exposed mice significantly inhibited B lymphocyte proliferation stimulated with LPS compared with AM from non-CS-exposed mice. Generations of superoxide and hydrogen peroxide were significantly increased in CS-exposed AM compared with non-CS-exposed AM. Inhibition of B lymphocyte proliferation stimulated with LPS by AM from CS-exposed mice was clearly recovered by superoxide dismutase and catalase. CONCLUSIONS: These results suggest that the inhibition by CS-exposed AM of LPS-induced B lymphocyte proliferation may be caused by the increased superoxide and hydrogen peroxide generation of CS. Therefore, these immunological inhibitions by CS could be associated with increased risk of pulmonary diseases.