In:
Annals of the New York Academy of Sciences, Wiley, Vol. 1070, No. 1 ( 2006-07), p. 405-410
Abstract:
Abstract: Septic shock is a systemic response to severe bacterial infections, generally caused by Gram‐negative bacterial endotoxins, with multiple manifestations such as hypotension, tissue injury, disseminated intravascular coagulation, and multi‐organ failure. All these effects, are induced by the generation of pro‐inflammatory and vasodilator mediators, cell adhesion molecules, coagulation factors, and acute‐phase proteins. Vasoactive intestinal polypeptide (VIP) and pituitary adenylate cyclase‐activating polypeptide (PACAP) are two immunopeptides with anti‐inflammatory properties exerted through type 1 and 2 VIP receptors (VPAC1 and VPAC2, respectively), and PACAP receptor (PAC1). The present results recapitulate the protective role of PAC1 in an experimental model of lethal endotoxemia using a knockout for the PAC1 receptor. Our results demonstrate that VIP and PACAP decrease lipopolysaccharide (LPS)‐induced interleukin‐6 (IL‐6) production, neutrophil infiltration and intercellular adhesion molecule‐1 (ICAM‐1), vascular cell adhesion molecule‐1 (VCAM‐1), and fibrinogen expression through PAC1 receptor, providing an advantage to design more specific drugs complementing standard intensive care therapy in septic shock.
Type of Medium:
Online Resource
ISSN:
0077-8923
,
1749-6632
DOI:
10.1196/annals.1317.053
Language:
English
Publisher:
Wiley
Publication Date:
2006
detail.hit.zdb_id:
2834079-6
detail.hit.zdb_id:
211003-9
detail.hit.zdb_id:
2071584-5
SSG:
11
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