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Vasoactive Intestinal Peptide Ameliorates Acute Myocarditis and Atherosclerosis by Regulating Inflammatory and Autoimmune Responses.
Benitez, Raquel; Delgado-Maroto, Virginia; Caro, Marta; Forte-Lago, Irene; Duran-Prado, Mario; O'Valle, Francisco; Lichtman, Andrew H; Gonzalez-Rey, Elena; Delgado, Mario.
Afiliação
  • Benitez R; Institute of Parasitology and Biomedicine Lopez-Neyra, Consejo Superior Investigaciones Cientificas, Granada 18016, Spain.
  • Delgado-Maroto V; Institute of Parasitology and Biomedicine Lopez-Neyra, Consejo Superior Investigaciones Cientificas, Granada 18016, Spain.
  • Caro M; Institute of Parasitology and Biomedicine Lopez-Neyra, Consejo Superior Investigaciones Cientificas, Granada 18016, Spain.
  • Forte-Lago I; Institute of Parasitology and Biomedicine Lopez-Neyra, Consejo Superior Investigaciones Cientificas, Granada 18016, Spain.
  • Duran-Prado M; School of Medicine, Castilla La Mancha University, Ciudad Real 13071, Spain.
  • O'Valle F; Department of Pathology, School of Medicine, University of Granada, Granada 18016, Spain; and.
  • Lichtman AH; Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
  • Gonzalez-Rey E; Institute of Parasitology and Biomedicine Lopez-Neyra, Consejo Superior Investigaciones Cientificas, Granada 18016, Spain.
  • Delgado M; Institute of Parasitology and Biomedicine Lopez-Neyra, Consejo Superior Investigaciones Cientificas, Granada 18016, Spain; mdelgado@ipb.csic.es.
J Immunol ; 200(11): 3697-3710, 2018 06 01.
Article em En | MEDLINE | ID: mdl-29669783
ABSTRACT
Vasoactive intestinal peptide (VIP) is a neuropeptide that exerts various vascular and cardioprotective functions and regulates immune function and inflammatory response at multiple levels. However, its role in inflammatory cardiovascular disorders is largely unknown. Myocarditis and atherosclerosis are two inflammatory and autoimmune cardiovascular diseases that cause important adverse circulatory events. In this study, we investigate the therapeutic effects of VIP in various well-established preclinical models of experimental autoimmune myocarditis and atherosclerosis. Intraperitoneal injection of VIP during the effector phase of experimental autoimmune myocarditis in susceptible BALB/c mice significantly reduced its prevalence, ameliorated signs of heart hypertrophy and injury, attenuated myocardial inflammatory infiltration, and avoided subsequent profibrotic cardiac remodeling. This effect was accompanied by a reduction of Th17-driven cardiomyogenic responses in peripheral lymphoid organs and in the levels of myocardial autoantibodies. In contrast, acute and chronic atherosclerosis was induced in apolipoprotein E-deficient mice fed a hyperlipidemic diet and subjected to partial carotid ligation. Systemic VIP treatment reduced the number and size of atherosclerotic plaques in carotid, aorta, and sinus in hypercholesterolemic mice. VIP reduced Th1-driven inflammatory responses and increased regulatory T cells in atherosclerotic arteries and their draining lymph nodes. VIP also regulated cholesterol efflux in macrophages and reduced the formation of foam cells and their presence in atherosclerotic plaques. Finally, VIP inhibited proliferation and migration of smooth muscle cells and neointima formation in a mouse model of complete carotid ligation. These findings encourage further studies aimed to assess whether VIP can be used as a pharmaceutical agent to treat heart inflammation and atherosclerosis.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Doenças Autoimunes / Peptídeo Intestinal Vasoativo / Autoimunidade / Aterosclerose / Inflamação / Miocardite Tipo de estudo: Prognostic_studies / Risk_factors_studies Limite: Animals Idioma: En Ano de publicação: 2018 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Doenças Autoimunes / Peptídeo Intestinal Vasoativo / Autoimunidade / Aterosclerose / Inflamação / Miocardite Tipo de estudo: Prognostic_studies / Risk_factors_studies Limite: Animals Idioma: En Ano de publicação: 2018 Tipo de documento: Article