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

Abstract

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.

Protective Immunity against Chlamydia psittaci Lung Infection Induced by a DNA Plasmid Vaccine Carrying CPSIT_p7 Gene Inhibits Dissemination in BALB/c Mice

“…Under certain circumstances, Chlamydia can transmit to animals or humans. In addition, cross-infection between different hosts can also be achieved, causing severe harm to human public health, agriculture, and animal husbandry [ 1 , 2 ]. An active and effective vaccine is the optimal program to prevent the widely spread chlamydial diseases [ 3 ].…”

Inhalable Gene Therapy and the Lung Surfactant Problem

“…Unfortunately, most respiratory diseases are neither originated nor localized in the pulmonary endothelium. More often, they involve cell types that are present in the airway epithelium (including chronic obstructive pulmonary disease, asthma, and cystic fibrosis) or the alveolar epithelium (such as pneumonia, lung adenocarcinomas, acute lung injury, and idiopathic pulmonary fibrosis) − (Figure ). Because many of these diseases occur as the result of inherited anomalies, RNA-carrying LNPs provide the unique opportunity to use techniques like gene editing, silencing, or replacement therapies to address the root cause of disease rather than just managing symptoms .…”