NLRP3 deficiency abrogates silica-induced neutrophil infiltration, pulmonary damage and fibrosis.

ABSTRACT:

Background

Silicosis is a progressive and often fatal occupational lung disease. The NLRP3 inflammasome is an innate immune sensor that is activated by silica. Accumulating evidence has implicated a role for NLRP3 in silicosis pathogenesis. In this study, we mechanistically elucidated the contribution of NLRP3 to silica-induced pulmonary disease.

Methods

The in vivo role of NLRP3 was investigated following intranasal delivery of 2 mg of silica or diluent alone to wildtype, NLRP3 reporter, and NLRP3-deficient mice. Protein expression, inflammation, and histopathology were analyzed in the lung.

Results

Intranasal administration of silica recapitulated the key pathological features of human silicosis, including nonresolving inflammation, the formation of silicotic nodule

SUBMITTER: Lam M 

PROVIDER: S-EPMC11929224 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature