Eicosanoids derived from cytochrome P450 pathway of arachidonic acid and inflammatory shock

• Published in: Prostaglandins & other lipid mediators Vol. 145; p. 106377
• Main Authors: Tunctan, Bahar, Senol, Sefika Pinar, Temiz-Resitoglu, Meryem, Guden, Demet Sinem, Sahan-Firat, Seyhan, Falck, John R., Malik, Kafait U.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.12.2019
• Subjects: Animal models; Arachidonic acid; CYP-derived eicosanoids; Inflammatory shock; Septic shock; CARS; eNOS; RNA; TRAF; C. rodentium; CLP; LT; HR; LX; PICS; Arachidonic acid; TNF; sGC; HETE; NF-κB; DHET; PPAR; MODS; RNS; mTOR; IB; iNOS; CYP; Staphylococcus aureus; AA; VSMCs; IL; CASP; i.p; MAPK; PKG; PON; TIRAP; AP; i.v; NCF; SIRS; VCAM; TGF; NOS; LOX; EET; MEK or MKK; 2-AG; NOX; ROS; CGRP; MAP; ERK; CRP; NADPH; NO; Animal models; 5,14-HEDGE; mRNA; RXR; LPS; IFN; ASC; NLR; sEH; miRNA; NLRP3; Pseudomonas aeruginosa; TLR; E. coli; Inflammatory shock; CD; ICAM; MOF; CCI; IKK; ECF; Septic shock; COX; PAMP; STAT; PAF; JAK; PDGF; PG; i.c.v; MyD; ICU; ALI; DAMP; TAK; CYP-derived eicosanoids
• ISSN: 1098-8823
• DOI: 10.1016/j.prostaglandins.2019.106377

•Shock is classified based on the: Hypovolemic, cardiogenic, obstructive, and vasodilatory.•Vasodilatory (vasoplegic, vasogenic, or distributive) shock may be inflammatory, neurogenic, or anaphylactic.•Septic shock is the most common form of vasodilatory shock leading to multiple organ dysfunction syndrome.•Eicosanoids derived from CYP pathway of AA have been implicated in the pathogenesis of inflammatory shock states.•Targeting eicosanoids derived from CYP pathway of AA may provide a novel therapeutic approach to inflammatory shock. Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock, the most common form of vasodilatory shock, is a subset of sepsis in which circulatory and cellular/metabolic abnormalities are severe enough to increase mortality. Inflammatory shock constitutes the hallmark of sepsis, but also a final common pathway of any form of severe long-term tissue hypoperfusion. The pathogenesis of inflammatory shock seems to be due to circulating substances released by pathogens (e.g., bacterial endotoxins) and host immuno-inflammatory responses (e.g., changes in the production of histamine, bradykinin, serotonin, nitric oxide [NO], reactive nitrogen and oxygen species, and arachidonic acid [AA]-derived eicosanoids mainly through NO synthase, cyclooxygenase, and cytochrome P450 [CYP] pathways, and proinflammatory cytokine formation). Therefore, refractory hypotension to vasoconstrictors with end-organ hypoperfusion is a life threatening feature of inflammatory shock. This review summarizes the current knowledge regarding the role of eicosanoids derived from CYP pathway of AA in animal models of inflammatory shock syndromes with an emphasis on septic shock in addition to potential therapeutic strategies targeting specific CYP isoforms responsible for proinflammatory/anti-inflammatory mediator production.