ArticleKidney international2016
The complement factor 5a receptor 1 has a pathogenic role in chronic inflammation and renal fibrosis in a murine model of chronic pyelonephritis.
Article in Kidney international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 63 citations in OpenAlex.
- Advances in Complement Research: from Pathophysiology to Precision Medicine.Physiology (Bethesda, Md.) · 2026Review
- IL-17B protects against uropathogenicMicrobiology spectrum · 2026Article
- Zidovudine in synergistic combination with nitrofurantoin or omadacycline:Antimicrobial agents and chemotherapy · 2024Article
- Macrophage-Induced Pro-Fibrotic Gene Expression in Tubular Cells after Ischemia/Reperfusion Is Paralleled but Not Directly Mediated by C5a/C5aR1 Signaling.Life (Basel, Switzerland) · 2024Article
- Cardiotrophin-1 therapy reduces disease severity in a murine model of glomerular disease.Physiological reports · 2024Article
- C5a/C5aR1 axis as a key driver promotes epithelial-to-mesenchymal transition in airway epithelial cells in silica nanoparticles-induced pulmonary fibrosis.International immunopharmacology · 2023Article
- Allometrically scaling tissue forces drive pathological foreign-body responses to implants via Rac2-activated myeloid cells.Nature biomedical engineering · 2023Article
- Complement System Inhibitory Drugs in a Zebrafish (International journal of molecular sciences · 2023Article
- Immune defenses in the urinary tract.Trends in immunology · 2023Review
- Blockade of C5aR1 alleviates liver inflammation and fibrosis in a mouse model of NASH by regulating TLR4 signaling and macrophage polarization.Journal of gastroenterology · 2023Article
- Therapeutic Potential of Targeting Complement C5a Receptors in Diabetic Kidney Disease.International journal of molecular sciences · 2023Review
- COVID-19 and Acute Kidney Injury.Critical care clinics · 2022Review
- Folic acid-mediated fibrosis is driven by C5a receptor 1-mediated activation of kidney myeloid cells.American journal of physiology. Renal physiology · 2022Article
- Role of Complement System in Kidney Transplantation: Stepping From Animal Models to Clinical Application.Frontiers in immunology · 2022Review
- The C5a/C5aR1 Axis Contributes to the Pathogenesis of Acute Cystitis Through Enhancement of Adhesion and Colonization of UropathogenicFrontiers in cellular and infection microbiology · 2022Article
- Identification of Hub Genes and Immune-Related Pathways for Membranous Nephropathy by Bioinformatics Analysis.Frontiers in physiology · 2022Article
- Inhibition of fibroblast growth factor-inducible 14 attenuates experimental tubulointerstitial fibrosis and profibrotic factor expression of proximal tubular epithelial cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Article
- Staphylococcal Panton-Valentine Leucocidin and Gamma Haemolysin Target and Lyse Mature Bone Marrow Leucocytes.Toxins · 2020Article
- The C5a/C5aR2 axis promotes renal inflammation and tissue damage.JCI insight · 2020Article
- Deposition of the Membrane Attack Complex in Healthy and Diseased Human Kidneys.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Complement factor 5a (C5a) interaction with its receptor (C5aR1) contributes to the pathogenesis of inflammatory diseases, including acute kidney injury. However, its role in chronic inflammation, particularly in pathogen-associated disorders, is largely unknown. Here we tested whether the development of chronic inflammation and renal fibrosis is dependent on C5aR1 in a murine model of chronic pyelonephritis. C5aR1-deficient (C5aR1-/-) mice showed a significant reduction in bacterial load, tubule injury and tubulointerstitial fibrosis in the kidneys following infection, compared with C5aR1-sufficient mice. This was associated with reduced renal leukocyte infiltration specifically for the population of Ly6Chi proinflammatory monocytes/macrophages and reduced intrarenal gene expression of key proinflammatory and profibrogenic factors in C5aR1-/- mice following infection. Antagonizing C5aR1 decreased renal bacterial load, tissue inflammation and tubulointerstitial fibrosis. Ex vivo and in vitro studies showed that under infection conditions, C5a/C5aR1 interaction upregulated the production of proinflammatory and profibrogenic factors by renal tubular epithelial cells and monocytes/macrophages, whereas the phagocytic function of monocytes/macrophages was down-regulated. Thus, C5aR1-dependent bacterial colonization of the tubular epithelium, C5a/C5aR1-mediated upregulation of local inflammatory responses to uropathogenic E. coli and impairment of phagocytic function of phagocytes contribute to persistent bacterial colonization of the kidney, chronic renal inflammation and subsequent tubulointerstitial fibrosis.
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Registered trials
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