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MME MARIE-HELENE ARDITI

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Auteur de référence en rhumatologie
39 articles scientifiques publiés — un praticien à la pointe de la recherche

Rhumatologue

RPPS 10001926152

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Top publications · les plus citées

Kawasaki disease: pathophysiology and insights from mouse models

Nature reviews. Rheumatology · 2020

📚 241 citations🎯 RCR 13.87Top 1% NIH🔓 Open Access📄 PDF gratuit ↗

Interleukin-1β is crucial for the induction of coronary artery inflammation in a mouse model of Kawasaki disease

Circulation · 2012

📚 198 citations🎯 RCR 5.62Top 6% NIH🔓 Open Access📄 PDF gratuit ↗

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Background— Kawasaki disease (KD) is the most common cause of acute vasculitis and acquired cardiac disease in US children. Untreated, children may develop coronary artery aneurysms, myocardial infarction, and sudden death as a result of the illness. Up to a third of KD patients fail to respond to intravenous immunoglobulin, the standard therapy, and alternative treatments are being investigated. Genetic studies have indicated a possible role for interleukin (IL)-1β in KD. We therefore explored the role of IL-1β in a murine model of KD. Methods and Results— Using an established mouse model of KD that involves injection of Lactobacillus casei cell wall extract (LCWE), we investigated the role of IL-1β and caspase-1 (activated by the inflammasome and required for IL-1β maturation) in coronary arteritis and evaluated the efficacy of IL-1 receptor antagonist as a potential treatment. LCWE-induced IL-1β maturation and secretion were dependent on the NLRP3 inflammasome in macrophages. Both caspase-1–deficient and IL-1 receptor–deficient mice were protected from LCWE-induced coronary lesions. Injection of recombinant IL-1β into caspase-1–deficient mice restored the ability of LCWE to cause coronary lesions in response to LCWE. Furthermore, daily injections of the IL-1 receptor antagonist prevented LCWE-mediated coronary lesions up to 3 days after LCWE injection. Conclusions— Our results strongly suggest that caspase-1 and IL-1β play critical roles in the development of coronary lesions in this KD mouse model, blocked by IL-1 receptor antagonist. Therefore, anti–IL-1β treatment strategies may constitute an effective, more targeted treatment of KD to prevent coronary lesions.

Role of Interleukin-1 Signaling in a Mouse Model of Kawasaki Disease-Associated Abdominal Aortic Aneurysm

Arteriosclerosis, thrombosis, and vascular biology · 2016

📚 98 citations🎯 RCR 3.47Top 13% NIH🔓 Open Access📄 PDF gratuit ↗

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Objective— Kawasaki disease (KD) is the most common cause of acquired cardiac disease in US children. In addition to coronary artery abnormalities and aneurysms, it can be associated with systemic arterial aneurysms. We evaluated the development of systemic arterial dilatation and aneurysms, including abdominal aortic aneurysm (AAA) in the Lactobacillus casei cell-wall extract (LCWE)–induced KD vasculitis mouse model. Methods and Results— We discovered that in addition to aortitis, coronary arteritis and myocarditis, the LCWE-induced KD mouse model is also associated with abdominal aorta dilatation and AAA, as well as renal and iliac artery aneurysms. AAA induced in KD mice was exclusively infrarenal, both fusiform and saccular, with intimal proliferation, myofibroblastic proliferation, break in the elastin layer, vascular smooth muscle cell loss, and inflammatory cell accumulation in the media and adventitia. Il1r −/− , Il1a −/− , and Il1b −/− mice were protected from KD associated AAA. Infiltrating CD11c + macrophages produced active caspase-1, and caspase-1 or NLRP3 deficiency inhibited AAA formation. Treatment with interleukin (IL)-1R antagonist (Anakinra), anti–IL-1α, or anti–IL-1β mAb blocked LCWE-induced AAA formation. Conclusions— Similar to clinical KD, the LCWE-induced KD vasculitis mouse model can also be accompanied by AAA formation. Both IL-1α and IL-1β play a key role, and use of an IL-1R blocking agent that inhibits both pathways may be a promising therapeutic target not only for KD coronary arteritis, but also for the other systemic arterial aneurysms including AAA that maybe seen in severe cases of KD. The LCWE-induced vasculitis model may also represent an alternative model for AAA disease.

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MME MARIE-HELENE ARDITI

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Top publications · les plus citées

Publications scientifiques (39) — classées par pathologie

Transversal30

Pédiatrie4

Microbiote3

Revue générale2

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