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PAC1 Receptor
Author(s) -
MARTÍNEZ CARMEN,
ARRANZ ALICIA,
JUARRANZ YASMINA,
ABAD CATALINA,
GARCÍAGÓMEZ MARÍA,
ROSIGNOLI FLORENCIA,
LECETA JAVIER,
GOMARIZ ROSA P.
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1317.053
Subject(s) - septic shock , receptor , lipopolysaccharide , disseminated intravascular coagulation , sepsis , vasoactive intestinal peptide , cell adhesion molecule , fibrinogen , intercellular adhesion molecule 1 , immunology , chemistry , medicine , neuropeptide
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.