Endothelin-1 and its role in the pathogenesis of infectious diseases

LIFE SCIENCES

卷:118

Review

Freeman, Brandi D.¹  Machado, Fabiana S.²  Tanowitz, Herbert B.^1,3  Desruisseaux, Mahalia S.^1,3 

[1] Yeshiva Univ Albert Einstein Coll Med, Dept Pathol, Bronx, NY 10461 USA

[2] Univ Fed Minas Gerais, Fac Med, Inst Biol Sci, Dept Biochem & Immunol, Belo Horizonte, MG, Brazil

[3] Yeshiva Univ Albert Einstein Coll Med, Dept Med, Bronx, NY 10461 USA

关键词: Endothelin;    Blood brain barrier;    Inflammation;    Parasitic disease;    Sepsis;    Pneumonia;    Neuroinflammation;   

DOI  :  10.1016/j.lfs.2014.04.021

来源: Elsevier

【 摘 要 】

Endothelins are potent regulators of vascular tone, which also have mitogenic, apoptotic, and immunomodulatory properties (Rubanyi and Polokoff, 1994; Kedzierski and Yanagisawa. 2001; Bagnato et al., 2011). Three isoforms of endothelin have been identified to date, with endothelin-1 (ET-1) being the best studied. ET-1 is classically considered a potent vasoconstrictor. However, in addition to the effects of ET-I on vascular smooth muscle cells, the peptide is increasingly recognized as a pro-inflammatory cytokine (Teder and Noble, 2000; Sessa et al., 1991). ET-1 causes platelet aggregation and plays a role in the increased expression of leukocyte adhesion molecules, the synthesis of inflammatory mediators contributing to vascular dysfunction. High levels of ET-1 are found in alveolar macrophages, leukocytes (Sessa et al., 1991) and fibroblasts (Gu et al., 1991). Clinical and experimental data indicate that ET-1 is involved in the pathogenesis of sepsis (Tschaikowsky et al., 2000; Coto et al., 2012), viral and bacterial pneumonia (Schuetz et al.. 2008; Samransamruajkit et al., 2002). Rickettsia conorii infections (Davi et al., 1995), Chagas disease (Petkova et al., 2000, 2001), and severe malaria (Dai et al., 2012; Machado et al., 2006; Wenisch et al., 1996a; Dietmann et al., 2008). In this minireview, we will discuss the role of endothelin in the pathogenesis of infectious processes. (C) 2014 Elsevier Inc. All rights reserved.

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