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Alveolar macrophage phagocytic kinetics following pulmonary parainfluenza-3 virus infection
Abstract:
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) TCID50 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 less than 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 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 PAM from calves with viral pneumonitis had a lower Vmax than PAM from control calves, but that Km values were comparable. No differences in PAM 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 PAM phagocytic functions would be expected to depress pulmonary particulate clearance and lung defense mechanisms.
Insights
Parainfluenza-3 virus infection in calves impairs pulmonary alveolar macrophage function, reducing their ability to clear pathogens and defend the lungs. This study highlights depressed phagocytic activity in PI-3 virus-inflamed lungs.
Area of Science:
- Veterinary Immunology
- Respiratory Virology
- Cellular Pathology
Background:
- Bovine respiratory disease complex (BRDC) is a significant economic concern in the cattle industry.
- Parainfluenza-3 virus (PI-3) is a primary viral agent implicated in BRDC, leading to pneumonia.
- Pulmonary alveolar macrophages (PAM) are critical for lung defense against pathogens.
Purpose of the Study:
- To investigate the impact of experimental parainfluenza-3 virus (PI-3) infection on the cellular components of bronchoalveolar washings in calves.
- To evaluate the phagocytic function of pulmonary alveolar macrophages (PAM) in PI-3 virus-induced pneumonitis.
- To determine if PI-3 virus infection affects PAM's capacity to clear particulate matter and maintain lung defense.
Main Methods:
- Calves were experimentally infected with PI-3 virus via intranasal aerosol exposure.
- Bronchoalveolar cells were collected 7 days post-infection using volume-controlled bronchopulmonary lavage.
- Cellular analysis included enumeration, differential counts, and assessment of PAM phagocytic activity using bead assays and kinetic studies.
Main Results:
- PI-3 virus-infected calves exhibited transient tachypnea, pyrexia, and typical viral pneumonitis lesions.
- Elevated total lavage cell yield and neutrophil percentages were observed in infected calves.
- Significantly decreased phagocytic rates and Vmax were found in PAM from PI-3 infected calves compared to controls.
Conclusions:
- Experimental PI-3 virus infection depresses the phagocytic function of pulmonary alveolar macrophages in calves.
- Impaired PAM phagocytosis in PI-3 virus-induced pneumonitis compromises lung defense mechanisms.
- These findings underscore the role of PI-3 virus in weakening the lung's ability to clear foreign particles and fight infection.