The crucial role of NLRP3 inflammasome in viral infection-associated fibrosing interstitial lung diseases

Wiwin Is Effendi, Tatsuya Nagano

Research output: Contribution to journalReview articlepeer-review

14 Citations (Scopus)

Abstract

Idiopathic pulmonary fibrosis (IPF), one of the most common fibrosing interstitial lung diseases (ILD), is a chronic-age-related respiratory disease that rises from repeated micro-injury of the alveolar epithelium. Environmental influences, intrinsic factors, genetic and epigenetic risk factors that lead to chronic inflammation might be implicated in the development of IPF. The exact triggers that initiate the fibrotic response in IPF remain enigmatic, but there is now increasing evidence supporting the role of chronic exposure of viral infection. During viral infection, activation of the NLRP3 inflammasome by integrating multiple cellular and molecular signaling implicates ro-bust inflammation, fibroblast proliferation, activation of myofibroblast, matrix deposition, and ab-errant epithelial-mesenchymal function. Overall, the crosstalk of the NLRP3 inflammasome and viruses can activate immune responses and inflammasome-associated molecules in the development, progression, and exacerbation of IPF.

Original languageEnglish
Article number10447
JournalInternational Journal of Molecular Sciences
Volume22
Issue number19
DOIs
Publication statusPublished - 1 Oct 2021

Keywords

  • Chronic respiratory diseases
  • IL-1β and IL-18
  • Idiopathic pulmonary fibrosis
  • Inflammation
  • NLRP3 inflammasome
  • Viral infection

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