ArticleFrontiers in immunology2018
The Plasma Kallikrein-Kininogen Pathway Is Critical in the Pathogenesis of Colitis in Mice.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Multi-omics profiling reveals sphingolipid metabolism reprogramming of tumor-conditioned MDSCs in cervical cancer.BMC cancer · 2026Article
- The immunomodulatory potential of bradykinin signaling in autoimmune conditions.Frontiers in immunology · 2026Review
- An antibody targeting high-molecular-weight kininogen blocks contact system activation in a model of polymicrobial sepsis.Journal of thrombosis and haemostasis : JTH · 2025Article
- Dextran sodium sulfate-induced colitis in male BALB/c mice leads to albuminuria and increased markers of inflammation and tissue damage in the kidney.Physiological reports · 2025Article
- Therapeutic effect and mechanism of Ento-PB on ulcerative colitis in BALB/c mice induced by sodium dextran sulfate.Heliyon · 2024Article
- Inflammation: The Link between Neural and Vascular Impairment in the Diabetic Retina and Therapeutic Implications.International journal of molecular sciences · 2023Review
- Anti-HK antibody inhibits the plasma contact system by blocking prekallikrein and factor XI activation in vivo.Blood advances · 2023Article
- Dual viscosity mixture vehicle for intratympanic steroid treatment modifies the ROS and inflammation related proteomes.Frontiers in pharmacology · 2023Article
- Editorial: Kallikrein-kinin system: insights into a multifunctional system.Frontiers in physiology · 2023Article
- Tandem Mass Tag Analysis of the Effect of the Anterior Cingulate Cortex in Nonerosive Reflux Disease Rats with Shugan Jiangni Hewei Granules Treatment.Computational and mathematical methods in medicine · 2022Article
- The contact activation system and vascular factors as alternative targets for Alzheimer's disease therapy.Research and practice in thrombosis and haemostasis · 2021Article
- Gut Inflammation Induced by Dextran Sulfate Sodium Exacerbates Amyloid-β Plaque Deposition in the AppNL-G-F Mouse Model of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2021Article
- Article
- A Proteomics-Based Approach Reveals Differential Regulation of Urine Proteins between Metabolically Healthy and Unhealthy Obese Patients.International journal of molecular sciences · 2019Article
- The Gut-Kidney Axis: Putative Interconnections Between Gastrointestinal and Renal Disorders.Frontiers in endocrinology · 2018Review
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Authors and funding
8 authors.
Funding
Abstract
The kallikrein-kinin system (KKS) consists of two serine proteases, prekallikrein (pKal) and factor XII (FXII), and a cofactor, high-molecular-weight kininogen (HK). Upon activation of the KKS, HK is cleaved to release bradykinin. Although the KKS is activated in humans and animals with inflammatory bowel disease (IBD), its role in the pathogenesis of IBD has not been characterized. In the present study, we determined the role of the KKS in the pathogenesis of IBD using mice that lack proteins involved in the KKS. In two colitis models, induced by dextran sulfate sodium (DSS) or 2,4,6-trinitrobenzene sulfonic acid (TNBS), mice deficient in HK, pKal, or bradykinin receptors displayed attenuated phenotypes, including body weight loss, disease activity index, colon length shortening, histological scoring, and colonic production of cytokines. Infiltration of neutrophils and inflammatory monocytes in the colonic lamina propria was reduced in HK-deficient mice. Reconstitution of HK-deficient mice through intravenous injection of HK recovered their susceptibility to DSS-induced colitis, increased IL-1β levels in the colon tissue and bradykinin concentrations in plasma. In contrast to the phenotypes of other mice lacking other proteins involved in the KKS, mice lacking FXII had comparable colonic inflammation to that observed in wild-type mice. The concentration of bradykinin was significantly increased in the plasma of wild-type mice after DSS-induced colitis.
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