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Alveolar Macrophage Phagocytic Kinetics Following Pulmonary Parainfluenza‐3 Virus Infection
Author(s) -
Slauson David O.,
Lay John C.,
Castleman William L.,
Neilsen Nancy R.
Publication year - 1987
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.41.5.412
Subject(s) - bronchoalveolar lavage , biology , alveolar macrophage , virus , lung , immunology , pneumonitis , pulmonary alveolus , phagocytosis , bronchiolitis , macrophage , in vitro , medicine , biochemistry
Qualitative and quantitative evaluations of the cellular components of bronchoalveolar washings of calves with experimental parainfluenza‐3 virus pneumonitis and control calves were made. Calves were exposed to 10 9 TCID 50 of PI‐3 by intranasal aerosol exposure and bronchoalveolar cells obtained 7 days after infection by volume‐controlled bronchopulmonary lavage. Transient tachypnea and pyrexia occurred in all infected calves, and virus was recoverable at 7 days from nasal swabs and lung tissue. Pulmonary lesions were typical of viral pneumonitis, characterized by patchy alveolitis and bronchiolitis with accumulations of cells and inflammatory debris. The mean total lavage cell yield was elevated in the virus‐infected calves, and the percentage of neutrophils was elevated (P < 0.05). Increased numbers of pulmonary alveolar macrophages (PAM) were also recovered but the difference was not significant. Linear regression equations showed that a decreased proportion of PAM from virus‐infected animals were phagocytic. The mean initial phagocytic rates of macrophages from calves with viral pneumonitis were significantly decreased (P < 0.05) over controls. This difference was concentration dependent and required a phagocytic stimulus in excess of 12.5 × 10 6 beads/ml. Studies of phagocytic kinetics showed that PAM from calves with viral pneumonitis had a lower V max than PAM from control calves, but that K m values were comparable. No differences in PAM β‐glucuronidase and acid phosphatase activity were observed. These results indicate depressed phagocytic function in PI‐3 virus‐inflamed lungs relative to controls. In concert with virus‐induced airway lesions, such in vivo depression of PAM phagocytic functions would be expected to depress pulmonary particulate clearance and lung defense mechanisms.