Bronchial fibroblasts help regulate the inflammatory and immune microenvironment. However, the role of house dust mite (HDM)-induced bronchial fibroblasts in asthma-related airway inflammation remains unclear. In this study, stimulation of primary human bronchial fibroblasts with HDM, gene expression profiling, and differentially expressed gene (DEG) analysis revealed the expression of multiple inflammation-related cytokines, including interleukin (IL)-6, IL-1β, TNF superfamily member 15, C-C motif chemokine ligand 2, chemokine (C-X-C motif) ligand 1 (CXCL1), CXCL2, CXCL3, CXCL5, and CXCL6. Fibrosis-related genes of collagen type I alpha-2 chain, collagen type III alpha-1 chain, collagen type IV alpha-3 chain, and actin alpha 2 remained unchanged. Fibronectin, collagen type I alpha-1 chain (COL1A1), vimentin, and transforming growth factor beta 1 (TGFβ1) were downregulated, albeit with fold changes below 1.5. Gene ontology enrichment analysis indicated that these DEGs were closely associated with programmed cell death pathways, inflammatory signaling, neutrophils, Th2 cells, and eosinophils. Western blot analysis revealed that HDM stimulation did not alter the expression of vimentin or α-smooth muscle actin in bronchial fibroblasts, while fibronectin, COL1A1, and TGFβ1 levels were significantly reduced. HDM stimulation activated the NF-κB signaling pathway and markedly increased inflammatory cytokine expression and secretion in bronchial fibroblasts. These findings suggest that HDM-induced bronchial fibroblasts contribute to the development of asthma-related airway inflammation.
Experimental study
Not applicable
Bronchial Fibroblasts Respond to House Dust Mite Challenge with Cytokine Secretion: Role in Allergic Airway Inflammation
28-Nov-2025
All authors declare no commercial or financial conflict of interest in this paper.