[Temporal activation of cytokine-cytokine receptor interaction pathways in pulmonary fibrosis].

As a legally recognized occupational disease characterized by pulmonary fibrosis, silicosis involves complex pathogenic mechanisms. Nevertheless, the temporal sequence of the onset and progression of immune mechanisms underlying pulmonary fibrosis remains to be elucidated. This study aims to systematically elucidate the dynamic changes and underlying mechanisms of the cytokine-cytokine receptor interaction pathway during silicon dioxide-induced pulmonary fibrosis. A mouse model of pulmonary fibrosis was established using a natural inhalation exposure system, and temporal analyses were conducted through histopathological staining, transcriptome sequencing, and molecular biological validation. The results revealed that this pathway was persistently activated throughout the entire fibrotic process. The expression of key genes, such as CXCL1 and CXCL2, was temporally upregulated. Protein-level validation further confirmed that CXCL2 expression peaked at the mid-stage of dust exposure, while IL-33 protein levels progressively increased with the advancement of fibrosis, accompanied by the recruitment of inflammatory cells. The study concludes that the temporal activation of the cytokine-cytokine receptor interaction pathway is a core mechanism driving the progression of pulmonary fibrosis, providing a crucial theoretical basis for developing intervention strategies targeting immune pathways.