Endothelin-1 and its role in the pathogenesis of infectious diseases.
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-1 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; Goto 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.
Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA.
Brandi D
BD
Freeman
Departament of Biochemistry and Immunology, Institute of Biological Sciences, Faculty of Medicine, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Fabiana S
FS
Machado
Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA; Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, USA.
Herbert B
HB
Tanowitz
Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA; Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, USA. Electronic address: m.desruis@einstein.yu.edu.
Mahalia S
MS
Desruisseaux
D000818:Animals; D003141:Communicable Diseases / Q000209:etiology* / Q000378:metabolism*; D019332:Endothelin-1 / Q000378:metabolism*; D006801:Humans
D019332:Endothelin-1
Blood brain barrier; Endothelin; Inflammation; Neuroinflammation; Parasitic disease; Pneumonia; Sepsis