The role of fibroblast-neutrophil crosstalk in the pathogenesis of inflammatory diseases: a multi-tissue perspective
Neutrophil-fibroblast crosstalk drives inflammatory pathology across organ systems through both shared and tissue-specific mechanisms. This review synthesizes evidence from skin, lung, gut, cardiovascular, joint, sinus, and oral diseases, revealing conserved molecular pathways where fibroblasts secr...
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| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Frontiers Media S.A.
2025-05-01
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| Series: | Frontiers in Immunology |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fimmu.2025.1588667/full |
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| Summary: | Neutrophil-fibroblast crosstalk drives inflammatory pathology across organ systems through both shared and tissue-specific mechanisms. This review synthesizes evidence from skin, lung, gut, cardiovascular, joint, sinus, and oral diseases, revealing conserved molecular pathways where fibroblasts secrete chemokines (CXCL1/8/12) to recruit neutrophils, which, in turn, release neutrophil extracellular traps (NETs), elastase, and cytokines to modulate fibroblast function. Additionally, we identify critical tissue-specific differences, including the predominance of IL-36 signaling in COPD, IL-17-carrying NETs in systemic lupus erythematosus (SLE) and pulmonary fibrosis, and specialized fibroblast subpopulations, such as IDO1+ cells in CRSwNP and TNFRSF21+ cells in periodontitis. Translational insights highlight the therapeutic potential of targeting IL-17, NETs, and fibroblast subpopulations, though tissue-specific risks necessitate precision strategies. Future therapeutic efforts should focus on developing precision-targeted interventions that address organ-specific mechanisms to overcome treatment resistance in inflammatory disorders. |
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| ISSN: | 1664-3224 |