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

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133

Shuangyan Li1, Mingming Pan2, Hui Zhao3

  • 1Beijing Hospital, National Centre of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, 100730, Beijing, China.

Journal of Microbiology, Immunology, and Infection = Wei Mian Yu Gan Ran Za Zhi
|February 15, 2025
PubMed

Insights

Respiratory virus infections can cause lung fibrosis. Elevated chemokine (C-C motif) ligand 2 (CCL2) drives this fibrosis by recruiting inflammatory cells and increasing matrix proteins. Targeting the CCL2/CCR2 pathway may prevent lung scarring.

Area of Science:

  • Pulmonology
  • Virology
  • Immunology

Background:

  • Respiratory virus infections, including influenza and SARS-CoV-2, are significant causes of community and hospital-acquired pneumonia.
  • These infections can lead to severe pulmonary fibrosis, a condition gaining global attention post-COVID-19.
  • Inflammation triggered by respiratory viruses involves the production of proinflammatory mediators like chemokine (C-C motif) ligand 2 (CCL2).

Purpose of the Study:

  • To review common fibrosis sequelae following viral respiratory infections.
  • To discuss the role of elevated CCL2 levels in various respiratory virus infections.
  • To highlight the potential of targeting the CCL2/CCR2 axis for mitigating post-infection fibrosis.

Main Methods:

  • Literature review of studies on respiratory virus infections and pulmonary fibrosis.
  • Analysis of the role of CCL2 in inflammatory responses and fibrosis pathogenesis.
  • Discussion of therapeutic strategies targeting the CCL2/CCR2 axis.

Main Results:

  • Respiratory viruses are linked to significant pulmonary fibrosis sequelae.
  • Elevated CCL2 levels are consistently observed in various respiratory virus infections.
  • CCL2 is a critical chemokine involved in inflammatory cell recruitment and extracellular matrix production, promoting fibrosis.

Conclusions:

  • CCL2 plays a pivotal role in the pathogenesis of virus-induced pulmonary fibrosis.
  • Targeting the CCL2/CCR2 axis presents a promising therapeutic strategy for alleviating fibrosis after viral infections.
  • Further investigation into CCL2/CCR2 inhibition is warranted for managing post-viral lung scarring.
Keywords:
CCL2/CCR2 axisFibrosisrespiratory viruses

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