01973nas a2200385   4500000000100000008004100001260001300042653001800055653002100073653003200094653001000126653001600136653002600152653004400178653001400222653001600236653001100252653002000263653001200283653002500295653001200320653001800332653000900350653001700359653004100376100001200417700001700429700001300446700001300459245008400472300001100556490000700567520099900574022001401573       2006                            d  c2006 Jun10aBlood Vessels10aCyclooxygenase 210aCyclooxygenase 2 Inhibitors10aEdema10aEndothelium10aEosine Yellowish-(YS)10aGene Expression Regulation, Enzymologic10aGranuloma10aHematoxylin10aHumans10aImmunochemistry10aleprosy10aMycobacterium leprae10aNeurons10aNitrobenzenes10aSkin10aSulfonamides10aVascular Endothelial Growth Factor A1 aPesce C1 aGrattarola M1 aMenini S1 aFiallo P00aCyclooxygenase 2 expression in vessels and nerves in reversal reaction leprosy.  a1076-70 v743 a<p>Tissue expression of cyclooxygenase (COX)2, an inducible enzyme synthesizing eicosanoids in inflammation, was studied in reversal reaction (RR) leprosy in comparison with nonreactionary leprosy. COX2 was consistently expressed in cells of the mononuclear-macrophage lineage across the leprosy spectrum. Only in RR, the following two additional sites showed COX2 expression in the dermis and subcutis: 1) microvessels and 2) nerve bundles and isolated nerve fibers. The same sites also express vascular endothelial growth factor (VEGF). This is in keeping with experimental models relating VEGF to COX2 expression, with VEGF enhancing prostaglandin production through COX2 stimulation and prostaglandin synthase expression. We postulate that selective COX2 inhibitors, which are currently used in several inflammatory conditions, could be considered for RR treatment to reduce acute symptoms caused by tissue edema and possibly prevent long-term nerve damage, the main complication of RR.</p>  a0002-9637