Abstract
Aucte viral pneumonia predisposes both humans and experimental animals to secondary bacterial infection. One hypothesis is that defects exist in the phagocytic and killing function of alveolar macrophages (AM). To examine this hypothesis, AM function was evaluated during experimental viral pneumonia. Cotton rats (Sigmodon hispidus) inoculated with human parainfluenza type 3 virus (P3V) were sacrificed at selected points during infection and AM were collected by trans-tracheal saline lavage. To assess AM function, the cells were exposed in vitro to zymosan and their activity as indicated by light generation was measured. In P3V infected animals the total number of cells increased slightly by 72-96 hr. but there was a significant decrease in the chemiluminescent response (mean peak reduction, 55%). AM cultures inoculated with P3V did not become infected as determined by immunofluorescence; this suggests an indirect mechanism for the decreased chemiluminescence. AM metabolism may be suppressed since the luminescence of phagocytes is thought to be caused by extracellular release of oxygen radicals; alternately, the effect may be due to decreased phagocytosis of the zymosan. The findings support the premise that AM dysfunction plays a role in bacterial complications of P3V infections and perhaps of other respiratory viral diseases. (Supported by NHLBI SCOR Grant P50-HL19171.)
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
