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In Vivo Assessment of Alveolar Macrophage Efferocytosis Following Ozone Exposure
Published on: October 22, 2019
Alveolar macrophages are the main target cells in feline calicivirus-associated pneumonia
J M Monné Rodriguez1, T Soare2, A Malbon1
1Veterinary Pathology, School of Veterinary Science, University of Liverpool, Leahurst Campus, Chester High Road, Neston CH64 7TE, UK.
Abstract:
Feline calicivirus (FCV) is a pathogen of felids and one of the most common causative agents of feline upper respiratory disease (URD). Reports of natural FCV pneumonia in the course of respiratory tract infections are sparse. Therefore, knowledge on the pathogenesis of FCV-induced lung lesions comes only from experimental studies. The aim of the present study was to assess the type and extent of pulmonary involvement in natural respiratory FCV infections of domestic cats and to identify the viral target cells in the lung. For this purpose, histology, immunohistochemistry and RNA-in situ hybridisation for FCV and relevant cell markers were performed on diagnostic post-mortem specimens collected after fatal URD, virulent systemic FCV or other conditions. All groups of cats exhibited similar acute pathological changes, dominated by multifocal desquamation of activated alveolar macrophages (AM) and occasional type II pneumocytes with fibrin exudation, consistent with diffuse alveolar damage (DAD). In fatal cases, this was generally seen without evidence of epithelial regeneration. In cats without clinical respiratory signs, type II pneumocyte hyperplasia was present alongside the other changes, consistent with the post-damage proliferative phase of DAD. FCV infected and replicated in AM and, to a lesser extent, type II pneumocytes. This study shows that lung involvement is an infrequent but important feature of FCV-induced URD. AM are the main viral target cell and pulmonary replication site, and their infection is associated with desquamation and activation, as well as death via apoptosis.
Insights
Feline calicivirus (FCV) causes upper respiratory disease in cats. This study found FCV infects alveolar macrophages, leading to lung damage and apoptosis, even in mild infections.
Area of Science:
- Veterinary Pathology
- Virology
- Immunology
Background:
- Feline calicivirus (FCV) is a common cause of upper respiratory disease (URD) in cats.
- Natural FCV-induced pneumonia is rarely reported, with pathogenesis primarily studied experimentally.
- Understanding lung lesions and viral targets in natural FCV infections is crucial.
Purpose of the Study:
- To investigate pulmonary involvement in natural FCV infections.
- To identify the specific lung cells targeted by FCV.
- To correlate FCV infection with pathological changes in feline lungs.
Main Methods:
- Histopathology, immunohistochemistry, and RNA in situ hybridization were used.
- Diagnostic post-mortem specimens from cats with URD, systemic FCV, or other conditions were analyzed.
- FCV and cell markers were examined in lung tissues.
Main Results:
- Multifocal alveolar damage (DAD) characterized by macrophage and pneumocyte changes was observed.
- FCV primarily infected and replicated in alveolar macrophages (AM), and to a lesser extent, type II pneumocytes.
- Infected AM showed activation, desquamation, and apoptosis.
Conclusions:
- Lung involvement, though infrequent, is a significant aspect of FCV-induced URD.
- Alveolar macrophages are the primary viral target cells and replication sites in the feline lung.
- FCV infection of AM contributes to lung pathology and potentially fatal outcomes.
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