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Inhibition of interleukin-1ß signalling promotes atherosclerotic lesion remodelling in mice with inflammatory arthritis.
Dragoljevic, Dragana; Lee, Man Kit Sam; Louis, Cynthia; Shihata, Waled; Kraakman, Michael J; Hansen, Jacinta; Masters, Seth L; Hanaoka, Beatriz Y; Nagareddy, Prabhakara R; Lancaster, Graeme I; Wicks, Ian P; Murphy, Andrew J.
Afiliación
  • Dragoljevic D; Division of Immunometabolism Baker Heart and Diabetes Institute Melbourne VIC Australia.
  • Lee MKS; Department of Immunology Monash University Melbourne VIC Australia.
  • Louis C; Division of Immunometabolism Baker Heart and Diabetes Institute Melbourne VIC Australia.
  • Shihata W; Department of Immunology Monash University Melbourne VIC Australia.
  • Kraakman MJ; Inflammation Division Walter and Eliza Hall Institute of Medical Research Melbourne VIC Australia.
  • Hansen J; Division of Immunometabolism Baker Heart and Diabetes Institute Melbourne VIC Australia.
  • Masters SL; Division of Immunometabolism Baker Heart and Diabetes Institute Melbourne VIC Australia.
  • Hanaoka BY; Inflammation Division Walter and Eliza Hall Institute of Medical Research Melbourne VIC Australia.
  • Nagareddy PR; Inflammation Division Walter and Eliza Hall Institute of Medical Research Melbourne VIC Australia.
  • Lancaster GI; Department of Surgery Ohio State University Wexner Medical Center Columbus OH USA.
  • Wicks IP; Department of Surgery Ohio State University Wexner Medical Center Columbus OH USA.
  • Murphy AJ; Division of Immunometabolism Baker Heart and Diabetes Institute Melbourne VIC Australia.
Clin Transl Immunology ; 9(11): e1206, 2020.
Article en En | MEDLINE | ID: mdl-33204425
OBJECTIVES: Rheumatoid arthritis (RA), an inflammatory joint disorder, independently increases the risk of cardiovascular disease (CVD). IL-1ß contributes to both RA and CVD. We hypothesised that inhibiting IL-1 signalling with the IL-1R antagonist, anakinra, would dampen inflammation and promote resolution of atherosclerosis in arthritic mice. METHODS: Low-density lipoprotein receptor (Ldlr)-deficient mice were fed a Western-type diet for 14 weeks to develop atherosclerotic plaques. Mice were then switched to a chow diet, promoting lesion regression, and randomised to a control group or into groups where arthritis was induced by passive transfer of K/BxN arthritogenic serum. The arthritic mice were further randomised to vehicle or anakinra. RESULTS: Arthritis impaired atherosclerotic lesion regression when cholesterol was lowered. This was associated with a higher burden of plaque macrophages, likely due to monocytosis, driven by myelopoiesis in the bone marrow and spleen. Interestingly, delayed intervention with anakinra had no effect on arthritis in these mice. However, a significant improvement in atherosclerotic plaque remodelling to a more stable phenotype was observed. This was associated with fewer circulating monocytes, caused by a reduction in splenic extramedullary myelopoiesis. CONCLUSION: We show that inhibiting IL-1 signalling in arthritic mice with pre-existing atherosclerosis promotes lesion remodelling to a more stable phenotype, that is less likely to rupture and cause ischemic events such as myocardial infarction. This suggests that IL-1R antagonism may suppress CVD complications in patients with RA. Furthermore, inhibiting IL-1ß signalling in other patients with inflammatory diseases that also predispose to CVD may also benefit from anti-IL-1 therapy.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Clinical_trials Idioma: En Revista: Clin Transl Immunology Año: 2020 Tipo del documento: Article Pais de publicación: Australia

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Clinical_trials Idioma: En Revista: Clin Transl Immunology Año: 2020 Tipo del documento: Article Pais de publicación: Australia