Pulmonary inflammatory responses during viral pneumonia and secondary bacterial infection.

Abstract

Pulmonary bactericidal mechanisms are reduced during viral pneumonia. It has been proposed that secondary bacterial pneumonia occurs because the host's ability to mount an inflammatory response is suppressed. These studies examine the pathobiology of parainfluenza 1 virus and viral-associated staphylococcal pneumonia in a murine model. The sequence of leukocyte and fluid protein changes were studied in the lung and blood. An influx of polymorphonuclear leukocytes into the lungs occurred early in the viral infection, and coincided with lung macrophages aggregation. Maximal increases in pulmonary leukocytes occurred during the period associated with maximum suppression of lung bactericidal mechanisms (days 7-9). During this period, the host was capable of mounting an additional inflammatory response to staphyloccal challenges. Finally, viral pneumonia resulted in a prolonged elevation in the numbers of pulmonary macrophages, lymphocytes, and granulocytes. Thus, changes in lung biology persisted well after resolution of the initiating infections.