A role for bradykinin in the development of anti-collagen antibody-induced arthritis

Xie, Zhanli; Dai, Jihong; Yang, Aimei; Yu, Wu

doi:10.1093/rheumatology/keu015

Cited by 20 publications

(22 citation statements)

References 19 publications

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“…Bradykinin drives the inflammation in experimental models of osteoarthritis and neuroinflammation via upregulation of cytokines such as IL-1β 35,36 . Vice versa, IL-1β is known to augment the accumulation of bradykinin via upregulation of bradykinin receptors 37,38 and activation of prekallikrein-HMWK complexes 39 .…”

Section: Discussionmentioning

confidence: 99%

“…The prompt and striking clinical response to the bradykinin B2 receptor antagonist icatibant is in line with its efficacy in HAE patients and strongly supports our model of a bradykininmediated mechanism. Reasons for the persistence of mild arthralgia may be the short treatment duration of icatibant or the fact that bradykinin effects on joint inflammation are mediated via the B1 receptor rather than the B2 35 .…”

Section: Discussionmentioning

confidence: 99%

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Cold-induced urticarial autoinflammatory syndrome related to factor XII activation

et al. 2020

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Hereditary autoinflammatory diseases are caused by gene mutations of the innate immune pathway, e.g. nucleotide receptor protein 3 (NLRP3). Here, we report a four-generation family with cold-induced urticarial rash, arthralgia, chills, headache and malaise associated with an autosomal-dominant inheritance. Genetic studies identify a substitution mutation in gene F12 (T859A, resulting in p.W268R) which encodes coagulation factor XII (FXII). Functional analysis reveals enhanced autocatalytic cleavage of the mutated protein and spontaneous FXII activation in patient plasma and in supernatant of transfected HEK293 cells expressing recombinant W268R-mutated proteins. Furthermore, we observe reduced plasma prekallikrein, cleaved high molecular weight kininogen and elevated plasma bradykinin. Neutrophils are identified as a local source of FXII. Interleukin-1β (IL-1β) is upregulated in lesional skin and mononuclear donor cells exposed to recombinant mutant proteins. Treatment with icatibant (bradykinin-B2-antagonist) or anakinra (interleukin-1-antagonist) reduces disease activity in patients. In conclusion, our findings provide a link between contact system activation and cytokine-mediated inflammation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cold-induced urticarial autoinflammatory syndrome related to factor XII activation

et al. 2020

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“…Double-knockout mice that lacked 2 bradykinin receptors (B1RB2R 2/2 ) were described in our previous study (30). Mice that lacked FXII (FXII 2/2 ) were kindly provided by Dr. Frank Castellino (University of Notre Dame, Notre Dame, IN, USA).…”

Section: Animalsmentioning

confidence: 99%

“…KKS-knockout mice and their littermate control WT mice at 8 wk old with body weight between 20 and 24 g received intraperitoneal injections of 150 ml K/BxN serum on d 0 and 2. Ankle joint diameter was measured by using calipers (30).…”

Section: Generation Of K/bxn Serum and Induction Of K/bxn Serum Transmentioning

confidence: 99%

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A critical role for plasma kallikrein in the pathogenesis of autoantibody‐induced arthritis

et al. 2017

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The plasma kallikrein-kinin system (KKS) consists of serine proteases, prekallikrein (pKal) and factor XII (FXII), and a cofactor, high-MW kininogen (HK). Upon activation, activated pKal and FXII cleave HK to release bradykinin. Activation of this system has been noted in patients with rheumatoid arthritis, and its pathogenic role has been characterized in animal arthritic models. In this study, we generated 2 knockout mouse strains that lacked pKal and HK and determined the role of KKS in autoantibody-induced arthritis. In a K/BxN serum transfer-induced arthritis (STIA) model, mice that lacked HK, pKal, or bradykinin receptors displayed protective phenotypes in joint swelling, histologic changes in inflammation, and cytokine production; however, FXII-deficient mice developed normal arthritis. Inhibition of Kal ameliorated arthritis severity and incidence at early stage STIA and reduced the levels of major cytokines in joints. In addition to releasing bradykinin from HK, Kal directly activated monocytes to produce proinflammatory cytokines, up-regulated their C5aR and FcRIII expression, and released C5a. Immune complex increased pKal activity, which led to HK cleavage. The absence of HK is associated with a decrease in joint vasopermeability. Thus, we identify a critical role for Kal in autoantibody-induced arthritis with pleiotropic effects, which suggests that it is a new target for the inhibition of arthritis.-Yang, A., Zhou, J., Wang, B., Dai, J., Colman, R. W., Song, W., Wu, Y. A critical role for plasma kallikrein in the pathogenesis of autoantibody-induced arthritis.

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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

et al. 2017

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A role for bradykinin in the development of anti-collagen antibody-induced arthritis

Abstract: These 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.

Cited by 20 publications

References 19 publications

Cold-induced urticarial autoinflammatory syndrome related to factor XII activation

Cold-induced urticarial autoinflammatory syndrome related to factor XII activation

A critical role for plasma kallikrein in the pathogenesis of autoantibody‐induced arthritis

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

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