Atherosclerosis severity is not affected by a deficiency in IL‐33/ST2 signaling

Immunity, Inflammation and Disease

Praxedis Martin²  Gaby Palmer²  Emiliana Rodriguez²  Estelle Woldt²  Isabelle Mean²  Richard W. James³  Dirk E. Smith⁴  Brenda R. Kwak¹ 

[1] Department of Pathology and Immunology, School of Medicine, University of Geneva, Geneva, Switzerland;Division of Rheumatology, University Hospital of Geneva, Geneva, Switzerland;Division of Diabetes, Endocrinology and Nutrition, Department of Internal Medicine, University Hospital of Geneva, Geneva, Switzerland;Inflammation Research Department, Amgen Inc., Seattle, Washington, USA

关键词: Atherosclerosis;    IL‐33;    ST2;    Th1‐to‐Th2‐shift;   

DOI  :  10.1002/iid3.62

来源: Wiley

【 摘 要 】

Abstract

Interleukin (IL)-33 is a cytokine of the IL-1 family, which signals through the ST2 receptor. Previous work demonstrated that the systemic administration of recombinant IL-33 reduces the development of atherosclerosis in apolipoprotein E-deficient (ApoE^−/−) mice by inducing a Th1-to-Th2 shift. The objective of our study was to examine the role of endogenous IL-33 and ST2 in atherosclerosis. ApoE^−/−, IL-33^−/−ApoE^−/−, and ST2^−/−ApoE^−/− mice were fed with a cholesterol-rich diet for 10 weeks. Additionally, a group of ApoE^−/− mice was injected with a neutralizing anti-ST2 or an isotype control antibody during the period of the cholesterol-rich diet. Atherosclerotic lesion development was measured by Oil Red O staining in the thoracic-abdominal aorta and the aortic sinus. There were no significant differences in the lipid-staining area of IL-33^−/−ApoE^−/−, ST2^−/−ApoE^−/−, or anti-ST2 antibody-treated ApoE^−/− mice, compared to ApoE^−/− controls. The absence of IL-33 signaling had no major and consistent impact on the Th1/Th2 cytokine responses in the supernatant of in vitro-stimulated lymph node cells. In summary, deficiency of the endogenously produced IL-33 and its receptor ST2 does not impact the development of atherosclerosis in ApoE-deficient mice.

【 授权许可】

CC BY   
© 2015 The Authors. Immunity, Inflammation and Disease Published by John Wiley & Sons Ltd.

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