Influenza virus infection of human alveolar and blood-derived macrophages: differences in accessory cell function and interferon production.
Influenza virus infection in vitro depresses accessory cell function of human peripheral blood-derived macrophages (PBM phi) for lymphocyte proliferative responses, but effects on such functions of alveolar macrophages (AlvM phi) have not been described. AlvM phi were obtained by bronchoalveolar lavage from normal young volunteers, and the effects of influenza virus infection of AlvM phi and autologous PBM phi were compared by measuring the accessory support provided by these cells for phytohemagglutinin-induced proliferation of purified autologous lymphocytes. Accessory cell function of AlvM phi was not altered by viral infection; in contrast, this function was significantly depressed with autologous virus-infected PBM phi. Virus-infected PBM phi produced greater amounts of interferon than did autologous AlvM phi. However, synthesis of interferon or prostaglandins by virus-infected cells could not account, per se, for depression of lymphocyte responses in the presence of PBM phi. These studies detail functional heterogeneity of autologous PBM phi and AlvM phi in response to a common respiratory-tract pathogen, influenza virus.
D000328:Adult; D002478:Cells, Cultured; D005260:Female; D006801:Humans; D009980:Influenza A virus / Q000502:physiology*; D007370:Interferon Type I / Q000096:biosynthesis* / Q000502:physiology; D008213:Lymphocyte Activation; D008264:Macrophages / Q000276:immunology / Q000378:metabolism / Q000382:microbiology*; D008297:Male; D011453:Prostaglandins / Q000502:physiology; D011458:Prostaglandins E / Q000502:physiology; D011650:Pulmonary Alveoli / Q000166:cytology
D007370:Interferon Type I; D011453:Prostaglandins; D011458:Prostaglandins E