Blocking Toll-like receptor 9 attenuates bleomycin-induced pulmonary injury

Acute respiratory distress syndrome (ARDS) is one of the most common complications in coronavirus disease 2019 patients suffering from acute lung injury (ALI). In ARDS, marked distortion of pulmonary architecture has been reported. The pulmonary lesions in ARDS include hemodynamic derangements (such...

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Published inJournal of pathology and translational medicine Vol. 56; no. 2; pp. 81 - 91
Main Authors Alzahrani, Badr, Gaballa, Mohamed M S, Tantawy, Ahmed A, Moussa, Maha A, Shoulah, Salma A, Elshafae, Said M
Format Journal Article
LanguageEnglish
Published Korea (South) Korean Society of Pathologists, Korean Society for Cytopathology 01.03.2022
The Korean Society of Pathologists and the Korean Society for Cytopathology
Korean Society of Pathologists & the Korean Society for Cytopathology
대한병리학회
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Summary:Acute respiratory distress syndrome (ARDS) is one of the most common complications in coronavirus disease 2019 patients suffering from acute lung injury (ALI). In ARDS, marked distortion of pulmonary architecture has been reported. The pulmonary lesions in ARDS include hemodynamic derangements (such as alveolar edema and hemorrhage), vascular and bronchiolar damage, interstitial inflammatory cellular aggregations, and eventually fibrosis. Bleomycin induces ARDS-representative pulmonary damage in mice and rats; therefore, we used bleomycin model mice in our study. Recently, Toll-like receptor 9 (TLR9) was implicated in the development of ARDS and ALI. In this study, we evaluated the efficiency of a TLR9 blocker (ODN2088) on bleomycin-induced pulmonary damage. We measured the apoptosis rate, inflammatory reaction, and fibroplasia in bleomycin- and bleomycin + ODN2088-treated mice. Our results showed a significant amelioration in bleomycin-induced damage to pulmonary architecture following ODN2088 treatment. A marked decrease in pulmonary epithelial and endothelial apoptosis rate as measured by cleaved caspase-3 expression, inflammatory reaction as indicated by tumor necrosis factor α expression, and pulmonary fibrosis as demonstrated by Van Gieson staining and α-smooth muscle actin immunohistochemistry were observed following ODN2088 treatment. All these findings indicate that blocking downstream TLR9 signaling could be beneficial in prevention or mitigation of ARDS through hemodynamic derangements, inflammation, apoptosis, and fibrosis.
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ISSN:2383-7837
2383-7845
DOI:10.4132/jptm.2021.12.27