Work

The interplay between lung galectins and pro-fibrotic markers in post-COVID-19 fibrogenesis: A pilot study

Year: 2024

Type: article

Abstract: COVID-19, caused by the SARS-CoV-2 virus, can lead to serious lung conditions, notably interstitial pulmonary fibrosis. 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. 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. These findings suggest that galectins contribute to fibrotic progression following COVID-19 and highlight their potential as therapeutic targets. • COVID-19, caused by the SARS-CoV-2 virus, can result in interstitial pulmonary fibrosis. • The mechanism underlying the lung inflammation and scarring induced by SARS-CoV-2 is still unclear. • Human bronchoalveolar lavage samples post COVID-19 infection showed increased levels of profibrotic markers and galectins. • Galectins could be potential key players of pulmonary fibrosis post-SARS-CoV-2 infection.

Source: Life Sciences

DOI: 10.1016/j.lfs.2024.123326