Aims: COVID-19, caused by the SARS-CoV-2 virus, can lead to serious lung conditions, notably interstitial pulmonary fibrosis.
Main methods: Our study tracked the progression of fibrosis markers in serial bronchoalveolar lavage (BAL) measurements collected from 16 COVID-19 patients at 1, 3, and 6 months post-infection. Additionally, BAL samples from 10 healthy control subjects were included. Using RT-PCR, ELISA, and immunofluorescence, we monitored molecular markers of fibrosis and investigated the interplay between galectins-1 and -3 and key pro-fibrotic mediators.
Key findings: We found increased α-smooth muscle actin (αSMA)-positive macrophages and heightened levels of αSMA, TGFβ, and CTGF mRNA and proteins at six months compared to controls. Furthermore, galectin-1 and galectin-3 concentrations showed a time-dependent increase and correlated significantly with pro-fibrotic markers.
Significance: These findings suggest that galectins contribute to fibrotic progression following COVID-19 and highlight their potential as therapeutic targets.
Keywords: CTGF; Covid-19; Gal-1; Gal-3; Lung fibrosis; TGFβ; αSMA.
Copyright © 2024. Published by Elsevier Inc.