EFFECT OF INFLUENZA VIRAL-INFECTION ON INGESTION AND KILLING OF BACTERIA BY ALVEOLAR MACROPHAGES

Abstract

In experimental animals, influenza predisposes the lung to superinfection by reducing the antibacterial efficiency of the alveolar macrophage system. Becauase such defects may represent abnormalities in ingestion or inactivation of inhaled bacteria, these subcomponents of phagocytosis were tested in mice infected 5 days previously with influenza A virus (NWS or WSN). The mice were exposed to aerosols of Staphylococcus epidermidis and then the rates of bacterial inactivation and percentages of intracellularly located staphylococci were measured. Rates of bacterial inactivation were determined for the left lung by pour-plate enumeration methods. The percentage of ingested bacteria was determined in the in situ perfused right lung by histologically determining the intracellular or extracellular location of 100 or more staphylococci. Rates of inactivation of S. epidermidis at 4 h after bacterial challenge were control, 90.1%; WSN, 73.0%; NWS, 68.6% P < 0.01. The percentage of intracellular staphylococci at 4 h were control, 90.9%; WSN, 69.9%; and NWS, 73.8%, P < 0.01. Microcolonies of proliferating staphylococci were also observed within macrophages of mice infected with each strain of influenza. In this experimental model, influenzal infection apparently impairs the inactivation of inhaled bacteria by retarding the ingestion of bacteria and by allowing bacteria to proliferate within macrophages.