Eicosanoid imbalance in the NOD mouse is related to a dysregulation in soluble epoxide hydrolase and 15-PGDH expression.

Ann N Y Acad Sci 2006 Oct;1079:130-4

Department of Pathology, Immunology, and Laboratory Medicine, College of Medicine, University of Florida, 1600 SW Archer Road No. D11-41, Gainesville, FL 32610, USA.

Eicosanoids promote or resolve inflammation depending on the class produced. Macrophage from nonobese diabetic (NOD) mouse produce increased proinflammatory lipid mediators and low levels of antiinflammatory lipoxin A4 (LXA4). The enhanced proinflammatory eicosanoids is secondary to increased cyclooxygenase-2 (Cox-2) expression and low levels of prostaglandin/leukotriene catabolic enzyme, 15-hydroxyprostaglandin dehydrogenase (15-PGDH). Deficient LXA4 production is not due to deficient lipoxygenase (LO) activity, but is related to increased soluble epoxide hydrolase (sEH), involved in metabolism of anti-inflammatory epoxyeicosatrienoic acids (EET). These aberrations in eicosanoid biology suggest that inflammation in the NOD mouse is likely to be prolonged and robust and may contribute to type 1 diabetes (T1D) pathogenesis.

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http://dx.doi.org/10.1196/annals.1375.019DOI Listing
October 2006
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