ArticleLaboratory investigation; a journal of technical methods and pathology2015
The pathological role of IL-18Rα in renal ischemia/reperfusion injury.
Article in Laboratory investigation; a journal of technical methods and pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 31 citations in OpenAlex.
- Rac1 inhibition protects the kidney against kidney ischemia/reperfusion through the inhibition of macrophage migration.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Article
- Interplay of Good Bacteria and Central Nervous System: Cognitive Aspects and Mechanistic Considerations.Frontiers in neuroscience · 2021Review
- The adaptive immune response in cardiac arrest resuscitation induced ischemia reperfusion renal injury.Journal of biological research (Thessalonike, Greece) · 2020Article
- Foxp3-Positive Regulatory T Cells Contribute to Antifibrotic Effects in Renal Fibrosis via an Interleukin-18 Receptor Signaling Pathway.Frontiers in medicine · 2020Article
- NLRP3 inflammasome activation in platelets in response to sepsis.Physiological reports · 2019Article
- Protective Effects and Mechanisms of Shenhua Tablet () on Toll-Like Receptors in Rat Model of Renal Ischemia-Reperfusion Injury.Chinese journal of integrative medicine · 2019Article
- Role of IL-18 induced Amphiregulin expression on virus induced ocular lesions.Mucosal immunology · 2018Article
- The effect of whole-body cooling on renal function in post-cardiac arrest patients.BMC nephrology · 2017Observational
- Lipopolysaccharide-Induced Acute Kidney Injury Is Dependent on an IL-18 Receptor Signaling Pathway.International journal of molecular sciences · 2017Article
- Haemoadsorption reduces the inflammatory response and improves blood flow during ex vivo renal perfusion in an experimental model.Journal of translational medicine · 2017Article
- Signalling pathways involved in hypoxia-induced renal fibrosis.Journal of cellular and molecular medicine · 2017Review
- AnChemical science · 2017Article
- Impaired Fas-Fas Ligand Interactions Result in Greater Recurrent Herpetic Stromal Keratitis in Mice.Journal of immunology research · 2015Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin (IL)-18 is a proinflammatory cytokine produced by leukocytes and parenchymal cells (eg, tubular epithelial cells (TECs), mesangial cells, and podocytes). IL-18 receptor (IL-18R) is expressed on these cells in the kidney during ischemia/reperfusion injury (IRI), but its role in this injury is unknown. Fas/Fas ligand (FasL) is also involved in the pathogenesis of renal IRI via tubular apoptosis. In addition, IL-18 enhances the expression of FasL on TECs, but the mechanism underlying this enhancement is not known. Here we used IL-18Rα-deficient mice to explore the pathological role of IL-18Rα in renal IRI. We found that compared to wild-type (WT) mice with renal IRI as an acute kidney injury (AKI), the IL-18Rα-deficient mice demonstrated decreased renal function (as represented by blood urea nitrogen), tubular damage, an increased accumulation of leukocytes (CD4+ T cells, neutrophils, and macrophages), upregulated early AKI biomarkers (ie, urinary kidney injury molecule-1 levels), and increased mRNA expressions of proinflammatory cytokines (IL-1β, IL-12p40, and IL-18) and chemokines (intercellular adhesion molecule-1 and CCL2/monocyte chemoattractant protein-1). The mRNA expression of FasL in the kidney was increased in the IL-18Rα-deficient mice compared to the WT mice. The adoptive transfer of splenocytes by WT mice led to decreased renal IRI compared to the IL-18Rα-deficient mice. In vitro, the mRNA expression of FasL on TECs was promoted in the presence of recombinant IL-18. These data reveal that IL-18Rα has an anti-inflammatory effect in IRI-induced AKI. Above all, IL-18 enhanced the inflammatory mechanisms and the apoptosis of TECs through the Fas/FasL pathway by blocking IL-18Rα.
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