Alveolar macrophage phagocytic kinetics following pulmonary XXXX .

@entity291 @entity308 @entity55 @entity3794 @entity15609 @entity7405 @entity1800 @entity5924 @entity358 @entity221
Qualitative and quantitative evaluations of the cellular components of bronchoalveolar washings of @entity291 with experimental @entity15609 -3 virus @entity55 and control @entity291 were made. @entity291 were exposed to 10(9) TCID50 of PI-3 by intranasal aerosol exposure and bronchoalveolar cells obtained 7 days after infection by volume-controlled bronchopulmonary lavage. Transient @entity7405 and @entity221 occurred in all infected @entity291 , and virus was recoverable at 7 days from nasal swabs and lung tissue. Pulmonary lesions were typical of @entity1800 , characterized by patchy @entity3794 and @entity5924 with accumulations of cells and inflammatory debris. The mean total lavage cell yield was elevated in the virus-infected @entity291 , and the percentage of neutrophils was elevated (P less than 0.05). Increased numbers of @entity358 ( @entity358 ) were also recovered but the difference was not significant. Linear regression equations showed that a decreased proportion of @entity358 from virus-infected animals were phagocytic. The mean initial phagocytic rates of macrophages from @entity291 with @entity1800 were significantly decreased (P less than 0.05) over controls. This difference was concentration dependent and required a phagocytic stimulus in excess of 12.5 X 10(6) beads/ml. Studies of phagocytic kinetics showed that @entity358 from @entity291 with @entity1800 had a lower Vmax than @entity358 from control @entity291 , but that Km values were comparable. No differences in @entity358 beta-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 @entity358 phagocytic functions would be expected to @entity308 pulmonary particulate clearance and lung defense mechanisms.
