ArticleRheumatology (Oxford, England)2014
A role for bradykinin in the development of anti-collagen antibody-induced arthritis.
Article in Rheumatology (Oxford, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- The Coagulation Factors Fibrinogen, Thrombin, and Factor XII in Inflammatory Disorders-A Systematic Review.Frontiers in immunology · 2018Pooled it
- Cold-Induced Urticarias with Familial Background: Clinical Spectrum, Pathogenesis, and Diagnostic Challenges.Diagnostics (Basel, Switzerland) · 2025Review
- The Therapeutic Effects ofAntioxidants (Basel, Switzerland) · 2025Article
- Association between Toll-like receptor 9 signaling defect and developing post-infectious irritable bowel syndrome.Frontiers in immunology · 2025Article
- Endothelial cell sphingosine 1-phosphate receptor 1 restrains VE-cadherin cleavage and attenuates experimental inflammatory arthritis.JCI insight · 2024Article
- Receptor tyrosine kinases Tyro3, Axl, and Mertk differentially contribute to antibody-induced arthritis.Cell communication and signaling : CCS · 2023Article
- ATP spreads inflammation to other limbs through crosstalk between sensory neurons and interneurons.The Journal of experimental medicine · 2022Article
- Soluble CD13 induces inflammatory arthritis by activating the bradykinin receptor B1.The Journal of clinical investigation · 2022Article
- Identification of Human Kinin-Forming Enzyme Inhibitors from Medicinal Herbs.Molecules (Basel, Switzerland) · 2021Article
- Cold-induced urticarial autoinflammatory syndrome related to factor XII activation.Nature communications · 2020Article
- The Plasma Kallikrein-Kininogen Pathway Is Critical in the Pathogenesis of Colitis in Mice.Frontiers in immunology · 2018Article
- Development of a Novel Diagnostic Biomarker Set for Rheumatoid Arthritis Using a Proteomics Approach.BioMed research international · 2018Article
- Oxidative stress in inflammatory cells of patient with rheumatoid arthritis: clinical efficacy of dietary antioxidants.Inflammopharmacology · 2017Review
- A critical role for plasma kallikrein in the pathogenesis of autoantibody-induced arthritis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- An essential role of high-molecular-weight kininogen in endotoxemia.The Journal of experimental medicine · 2017Article
- Mixed effects of caffeic acid phenethyl ester (CAPE) on joint inflammation, bone loss and gastrointestinal inflammation in a murine model of collagen antibody-induced arthritis.Inflammopharmacology · 2017Article
- Factor XII-Driven Inflammatory Reactions with Implications for Anaphylaxis.Frontiers in immunology · 2017Review
- Contact pathway of coagulation and inflammation.Thrombosis journal · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
objectivesClinical and experimental observations have suggested that bradykinin, a major activation product of the plasma kallikrein-kinin system, is involved in the pathogenesis of arthritis, but the pathogenic role of bradykinin receptors remains inconclusive. In this study we examined whether bradykinin receptors are important in the pathogenesis of anti-collagen antibody-induced arthritis (CAIA) using double receptor-deficient (B1RB2R(-/-)) mice.
methodsCAIA was induced in B1RB2R(+/+) and B1RB2R(-/-) mice by injection of an anti-collagen antibody cocktail on day 0 and lipopolysaccharide on day 3. Severity of disease was evaluated by measurement of joint diameter and histological analysis. The expression of proinflammatory cytokines in joint tissue and peripheral mononuclear cells was determined by ELISA and real-time RT-PCR.
resultsThe absent expression of B1R and B2R mRNA in B1RB2R(-/-) mice was confirmed by RT-PCR. Although B1RB2R(+/+) mice developed severe CAIA, the severity of the disease was significantly attenuated in B1RB2R(-/-) mice. In B1RB2R(+/+) mice bearing CAIA, both B1R and B2R mRNA levels were increased in joint tissue and peripheral mononuclear cells. Compared with B1RB2R(+/+) mice, the production of IL-1β and IL-6 in joint tissue and their mRNA expression in peripheral mononuclear cells were remarkably reduced in B1RB2R(-/-) mice.
conclusionThese observations provide genetic evidence that bradykinin plays an important role in the pathogenesis of CAIA. B1R, whose expression is induced in inflamed joint tissue and peripheral inflammatory cells, is important in the development of CAIA.
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