Type II Alveolar Cells Play Roles in Macrophage-Mediated Host Innate Resistance to Pulmonary Mycobacterial Infections by Producing

Roles of type II pneumocytes in macrophage (Mf) – mediated host resistance to pulmonary Mycobacterium tuberculosis (MTB) and M. avium complex (MAC) infections were studied. Elec-tron microscopy of the lung sections of mice given intratracheal infection indicated that the or-ganisms invaded both Mfs and type II pneumocytes. When Mono-Mac-6 Mfs (MM6-Mfs) and A-549 type II pneumocytes (A-549 cells) were cocultivated, bacterial growth in MM6-Mfs was reduced by A-549 cell – derived soluble factors, indicating the roles of type II pneumocytes in Mf-mediated host resistance to mycobacteria. MTB- or MAC-infected A-549 cells showed in-creased mitochondrial RNA expression of cytokines and surfactant proteins (SPs), in the order tumor necrosis factor–a (TNF-a)> granulocyte-Mf colony-stimulating factor (GM-CSF). Mf chemoattractant protein> interleukin-8. SP-D. Anti–TNF-a and anti–GM-CSF antibodies attenuated A-549 cell – dependent inhibition of intramacrophage mycobacteria, indicating their crucial roles in A-549 cell–mediated potentiation of Mf antimycobacterial activity. Mycobacterium tuberculosis (MTB) and M. avium complex (MAC) are important pathogens that cause persistent pulmonary infections in humans. These pathogens also cause disseminate