ids. The conversion of DHA by leukocytes, brain, and glial cells to 17S-hydroxy-containing docosanoids denoted as docosatrienes and 17S series resolvins serve as regulators of both leukocytes reducing infiltration in vivo and glial cells blocking their cytokine production. These results indicate that DHA is the precursor to potent protective mediators generated via enzymatic oxygenations to novel docosatrienes and 17S series resolvins that have significant anti-inflammatory action and participate in the resolution of inflammatory events. Similar small molecular weight compounds are also generated from AA, EPA, and DHA: 15R-hydroxy containing compounds from AA, 18R series from EPA, and 17R-hydroxy series from DHA. All these compounds have potent anti-inflammatory actions, resolve inflammation and hence are called as “resolvins”. Resolvins inhibited cytokine generation, leukocyte recruitment, leukocyte diapedesis, and exudate formation. The formation of resolvins from AA, EPA, and DHA from acetylated COX-2 are generated via transcellular biosynthesis, and their main purpose appears to be to suppress inflammation. Resolvins inhibited brain ischemia-reperfusion injury. It is possible that lipoxins, resolvins and protectins behave as endogenous anti-inflammatory and cytoprotective molecules. The general cytoprotective properties that have been attributed to AA, EPA, and DHA can be related to their conversion to lipoxins, resolvins and docosanoids. Hence, any defect in the synthesis of lipoxins, resolvins and protectins or their inappropriate degradation could lead to perpetuation of inflammation as seen in lupus and other rheumatological conditions. Anti-inflammatory molecule lipoxin A4 is detectable in urine LX4, generated by lipoxygenase transformation of AA possess potent anti-inflammatory activity in vivo, and temporal biosynthesis of LX, concurrent with spontaneous resolution, has been observed during exudate formation. Recently, a new extraction technique, more selective for LX, which abolishes background Das Lipids in Health and Disease 2011, 10:76 http://www.lipidworld.com/content/10/1/76 Page 4 of 8 contamination and minimizes the unspecific reading, was developed. This new method showed that urine from healthy subjects contains LXA4. Subsequently, it was shown that strenuous exercise significantly increased urinary excretion in healthy volunteers. These findings confirm that alterations in the urinary excretion of LXA4 can used as a reflection of changes in its formation, 
especially in the kidney, to monitor changes in the systemic and renal inflammatory lesions. In a further extension of this work, it was reported that urinary levels of LXA4 was decreased while that of cysLTs increased in volunteers aged from 26 to over 100 years leading to a profound unbalance of the LXA/cysLTs ratio that may be considered an index of the endogenous anti-inflammatory potential. These results suggest that endogenous anti-inflammatory mechanisms become less efficient with age that could result in increased susceptibility to inflammatory disorders with advancing age. Urinary LXA4 is decreased and LTs increased in HSP nephritis or decreased levels of LXA4 that acts as a “stop signal” of inflammatory process may be LY3039478 responsible for the nephritis seen in HSP. Anti-inflammatory cytokines IL-4 and IL-10 enhance LXA4 synthesis In a study in which temporal changes of blood and urinary PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19797474 LXA4, LTB4 and urinary LTE4 was determined in 49 children with Henoch-Sch
