Lymphoproliferative responses to antigens mediated by human pulmonary alveolar macrophages.
We evaluated the ability of human pulmonary alveolar macrophages (PAMs) to mediate (3H)-thymidine incorporation by blood lymphocytes severely depleted of monocytes when stimulated with soluble microbial and allogeneic lymphocyte antigens. Low (less than 2%) concentrations of PAM's from nonsmokers or blood monocytes did not support optimal responses. Over all, at greater than or equal to 10% concentrations, PAM's from nonsmokers supported higher responses than monocytes. At less than or equal to 10% concentrations, PAM's from heavy cigarette smokers mediated significantly less incorporation than did similar concentrations of PAM's from nonsmokers (p less than 0.05). The findings indicate that PAM's from healthy nonsmokers are functionally competent macrophages in terms of mediating lymphoproliferation in cultures stimulated with antigens. This classical macrophage function is impaired with cigarette smoking.
D000328:Adult; D000941:Antigens / Q000008:administration & dosage; D006801:Humans; D007111:Immunity, Cellular; D007958:Leukocyte Count; D008213:Lymphocyte Activation; D008214:Lymphocytes / Q000378:metabolism; D008264:Macrophages / Q000276:immunology*; D009000:Monocytes / Q000276:immunology; D010587:Phagocytosis; D011650:Pulmonary Alveoli / Q000276:immunology*; D012907:Smoking / Q000503:physiopathology; D013936:Thymidine / Q000378:metabolism
D000941:Antigens; D013936:Thymidine