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Open AccessArticle

Regeneration of Pulmonary Tissue in a Calf Model of Fibrinonecrotic Bronchopneumonia Induced by Experimental Infection with Chlamydia psittaci

1
Institute for Molecular Pathogenesis, Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health, Naumburgerstr. 96a, 07743 Jena, Germany
2
Chemisches und Veterinäruntersuchungsamt Rhein-Ruhr-Wupper (CVUA-RRW), Deutscher Ring 100, 47798 Krefeld, Germany
3
Institute of Bioinformatics, Friedrich-Schiller-Universität Jena, Leutragraben 1, 07743 Jena, Germany
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(8), 2817; https://doi.org/10.3390/ijms21082817
Received: 19 February 2020 / Revised: 10 April 2020 / Accepted: 15 April 2020 / Published: 17 April 2020
(This article belongs to the Special Issue The Alveolar Epithelium: Mechanisms of Injury and Repair)
Pneumonia is a cause of high morbidity and mortality in humans. Animal models are indispensable to investigate the complex cellular interactions during lung injury and repair in vivo. The time sequence of lesion development and regeneration is described after endobronchial inoculation of calves with Chlamydia psittaci. Calves were necropsied 2–37 days after inoculation (dpi). Lesions and presence of Chlamydia psittaci were investigated using histology and immunohistochemistry. Calves developed bronchopneumonia at the sites of inoculation. Initially, Chlamydia psittaci replicated in type 1 alveolar epithelial cells followed by an influx of neutrophils, vascular leakage, fibrinous exudation, thrombosis and lobular pulmonary necrosis. Lesions were most extensive at 4 dpi. Beginning at 7 dpi, the number of chlamydial inclusions declined and proliferation of cuboidal alveolar epithelial cells and sprouting of capillaries were seen at the periphery of necrotic tissue. At 14 dpi, most of the necrosis had been replaced with alveoli lined with cuboidal epithelial cells resembling type 2 alveolar epithelial cells and mild fibrosis, and hyperplasia of organized lymphoid tissue were observed. At 37 dpi, regeneration of pulmonary tissue was nearly complete and only small foci of remodeling remained. The well-defined time course of development and regeneration of necrotizing pneumonia allows correlation of morphological findings with clinical data or treatment regimen. View Full-Text
Keywords: lung; pneumonia; necrotizing; regeneration; model; bovine; chlamydia lung; pneumonia; necrotizing; regeneration; model; bovine; chlamydia
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Liebler-Tenorio, E.M.; Lambertz, J.; Ostermann, C.; Sachse, K.; Reinhold, P. Regeneration of Pulmonary Tissue in a Calf Model of Fibrinonecrotic Bronchopneumonia Induced by Experimental Infection with Chlamydia psittaci. Int. J. Mol. Sci. 2020, 21, 2817.

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