ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014
Crosstalk between TGF-β1 and complement activation augments epithelial injury in pulmonary fibrosis.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 107 citations in OpenAlex.
- Complement C5a Promotes Epithelial-Mesenchymal Transition in Pterygium via C5aR Activation.Investigative ophthalmology & visual science · 2026Article
- Disease Mechanisms and Therapeutic Advances in Idiopathic and Progressive Pulmonary Fibrosis: From Approved Drugs to Emerging Strategies.Journal of clinical medicine · 2026Review
- Milk fat globule EGF and factor V/VIII domain containing (MFGE8) as a novel player in equine endometrial fibrosis.Scientific reports · 2026Article
- Expression of complement pathway genes is associated with progression of idiopathic pulmonary fibrosis.Respiratory research · 2026Article
- NAMPT orchestrates fibroblast cuproptosis and immune crosstalk during IPF progression.Frontiers in immunology · 2026Article
- Serum response factor is essential for endometrial function and prevention of inflammatory fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Single-cell transcriptomic analysis of blood and bronchoalveolar lavage fluid in progressive fibrosing interstitial lung diseases.Scientific reports · 2025Article
- ACSL4 Drives C5a/C5aR1-Calcium-Induced Fibroblast-to-Myofibroblast Transition in a Bleomycin-Induced Mouse Model of Pulmonary Fibrosis.Biomolecules · 2025Article
- Complement's involvement in allergic Th2 immunity: a cross-barrier perspective.The Journal of clinical investigation · 2025Review
- Immunobiology of pulmonary fibrosis.Frontiers in immunology · 2025Review
- Multi-Target Peptide Nanofiber Immunotherapy Diminishes Complement Anaphylatoxin Activity in Acute Inflammation.Advanced healthcare materials · 2025Article
- Complement Immune System in Pulmonary Hypertension-Cooperating Roles of Circadian Rhythmicity in Complement-Mediated Vascular Pathology.International journal of molecular sciences · 2024Review
- Ficolin-1 ameliorates pulmonary fibrosis via directly binding to TGF-β1.Journal of translational medicine · 2024Article
- A Histological Analysis and Detection of Complement Regulatory Protein CD55 in SARS-CoV-2 Infected Lungs.Life (Basel, Switzerland) · 2024Article
- Local complement activation and modulation in mucosal immunity.Mucosal immunology · 2024Review
- Review
- The complement cascade in lung injury and disease.Respiratory research · 2024Review
- A computational approach for the identification of key genes and biological pathways of chronic lung diseases: a systems biology approach.BMC medical genomics · 2023Article
- Antifibrotic mechanism of avitinib in bleomycin-induced pulmonary fibrosis in mice.BMC pulmonary medicine · 2023Article
- GlyPerA™ effectively shields airway epithelia from SARS-CoV-2 infection and inflammatory events.Respiratory research · 2023Article
3 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The epithelial complement inhibitory proteins (CIPs) cluster of differentiation 46 and 55 (CD46 and CD55) regulate circulating immune complex-mediated complement activation in idiopathic pulmonary fibrosis (IPF). Our previous studies demonstrated that IL-17A mediates epithelial injury via transforming growth factor β1 (TGF-β1) and down-regulates CIPs. In the current study, we examined the mechanistic role of TGF-β1 in complement activation-mediated airway epithelial injury in IPF pathogenesis. We observed lower epithelial CIP expression in IPF lungs compared to normal lungs, associated with elevated levels of complement component 3a and 5a (C3a and C5a), locally and systemically. In normal primary human small airway epithelial cells (SAECs) treated with TGF-β1 (10 ng/ml), C3a, or C5a (100 nM), we observed loss of CIPs and increased poly(ADP-ribose) polymerase (PARP) activation [also observed with RNA interference (RNAi) of CD46/CD55]. TGF-β1-mediated loss of CIPs and Snail induction [SNAI1; a transcriptional repressor of E-cadherin (E-CAD)] was blocked by inhibiting mitogen-activated protein kinase (p38MAPK; SB203580) and RNAi silencing of SNAI1. C3a- and C5a-mediated loss of CIPs was also blocked by p38MAPK inhibition. While C3a upregulated TGFb transcripts, both C3a and C5a down-regulated SMAD7 (negative regulator of TGF-β), and whereas TGF-β1 induced C3a/C5a receptor (C3aR/C5aR) expression, pharmacologic C3aR/C5aR inhibition protected against C3a-/C5a-mediated loss of CIPs. Taken together, our results suggest that epithelial injury in IPF can be collectively amplified as a result of TGF-β1-induced loss of CIPs leading to complement activation that down-regulates CIPs and induces TGF-β1 expression
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