Diethylcarbamazine (DEC) is an antifilarial drug with potent anti-inflammatory properties as a result of its interference with the metabolism of arachidonic acid. The aim of the present study was to evaluate the anti-inflammatory activity of DEC in a mouse model of acute inflammation (carrageenan-induced pleurisy). The injection of carrageenan into the pleural cavity induced the accumulation of fluid containing a large number of polymorphonuclear cells (PMNs) as well as infiltration of PMNs in lung tissues and increased production of nitrite and tumor necrosis factor-α and increased expression of interleukin-1β, cyclooxygenase (COX-2), and inducible nitric oxide synthase. Carrageenan also induced the expression of nuclear factor-κB. The oral administration of DEC (50？mg/Kg) three days prior to the carrageenan challenge led to a significant reduction in all inflammation markers. The present findings demonstrate that DEC is a potential drug for the treatment of acute lung inflammation. 1. Introduction Since 1947, diethylcarbamazine citrate (DEC) has been used in the treatment and control of lymphatic filariasis, which is caused by the nematodes Wuchereria bancrofti, Brugia malayi, and B. timori, and is one of the drugs used in the Global Programme for the Elimination of Lymphatic Filariasis [1]. However, despite its long period of use, little is known regarding its mechanism of action. Pharmacological studies have demonstrated that DEC affects the metabolism of arachidonic acid, thereby acting as an anti-inflammatory drug. Substantial evidence has demonstrated that DEC blocks a number of steps in both the cyclooxygenase (COX) and lipoxygenase pathways. This drug is a potent blocker of leukotriene production, and bronchial vasoconstrictor substances and also inhibits the production of prostaglandin (PGE2), prostacyclin (PGI2), and thromboxane A2 (TXA2) [2]. According to Mathews and Murphy (1982) [3], DEC inhibits the formation of LTB4 and sulfidopeptide leukotrienes, which are potent vaso/bronchoconstrictors, in mastocytomas, while stimulating the formation of 5-hydroxyeicosatetraenoic acid, suggesting that the site of action of DEC for inhibiting leukotrienes formation may be the leukotriene A4 synthetase reaction. Moreover, Bach and Brashler (1986) [4] found that DEC inhibited the formation of sulfidopeptide leukotrienes in rat basophil leukemia cells. Clinical studies have found that DEC is quite effective in the treatment of symptoms of bronchial asthma [5, 6]. Recent studies carried out in cooperation with our laboratory demonstrated that DEC plays an
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