Role of CCL2/CCR2 axis in pulmonary fibrosis induced by respiratory viruses

Abstract

Respiratory virus infection is an important cause of both community acquired pneumonia and hospital-acquired pneumonia. Various respiratory viruses, including influenza virus, avian influenza virus, respiratory syncytial virus (RSV), SARS-CoV, MERS-CoV, and SARS-CoV-2, result in severe fibrosis sequelae after the acute phase. Since the COVID-19 pandemic, respiratory virus infection, as an important cause of pulmonary fibrosis, has attracted increasing attention around the world. Respiratory virus infection usually triggers robust inflammation responses, leading to large amounts of proinflammatory mediator production, such as chemokine (C-C motif) ligand 2 (CCL2), a critical chemokine involved in the recruitment of various inflammatory cells. Moreover, CCL2 plays a pivotal role in the pathogenesis of fibrosis progression, through regulating recruitment of bone marrow-derived monocytes and increasing the expression of extracellular matrix proteins. This review provided a concise overview of the common fibrosis sequelae after virus infection. Then we discussed the elevated levels of CCL2 in various respiratory virus infection, underscoring its potent profibrotic role. Targeting the CCL2/CCR2 axis holds promise for alleviating fibrosis sequelae post-acute virus infection and warrants further investigation.