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  • br Conclusion The results of the present study demonstrate t


    Conclusion The results of the present study demonstrate that cysteinyl leukotrienes LTC4, LTD4 and LTE4 cause moderate to marked whereas the dihydroxy leukotriene LTB4 causes small muscle contraction in the stomach in vitro. The LTD4-induced contraction is mediated by CysLT1 in fundus but by CysLT1 and CysLT2 in antrum.
    Conflict of interest statement
    Acknowledgments This work was supported by National Science Council of Taiwan (NSC 97-2314-B-303-012-MY3), Buddhist Tzu Chi General Hospital, Hualien, and E-Da Hospital. The author thanks Yu-Shyuan Wang, Ling-Jung Chiu, Mei-Ling Chen and Cai-Jing Lee for their excellent technical assistance.
    Introduction Acute pyelonephritis remains to be one of the most frequent nosocomial infectious diseases and a leading cause of kidney failure worldwide. Regardless of the etiology of renal injury, with the local activation of cellular, immunologic and biochemical mediators of inflammation, renal parenchyma is destructed (Wislon, 1996). The inflammatory response involves alterations in the biosynthesis of locally acting cytokines, growth factors and eicosanoids, activation of the complement system, increase in the mao inhibitors of adhesion molecules, release of degradative enzymes, and generation of reactive oxygen radicals (Nassar and Badr, 1998). The early events during the acute stage of pyelonephritis, that are mostly localized to the site of infection and not yet systemic, may greatly influence the pathologic outcome of the disease (Shimamura, 1981, Bille and Glauser, 1982, Tardif et al., 1994). In the chronic phase, associated with the degree of inflammation, renal fibrosis and subsequently renal scars may result in end stage kidney disease (Badr, 1997). Thus, preventing or limiting the inflammation and oxidative renal damage during the acute phase should be considered as a major goal in the treatment of pyelonephritis. Based on the improved understanding of the mechanisms of acute inflammatory processes that occur in response to bacterial multiplication of the kidney parenchyma and pyelonephritic scarring (Meylan et al., 1989, Brooks et al., 1974), several pro-inflammatory mediators have been identified as therapeutic targets, which suggest novel therapeutic strategies in limiting severity of pyelonephritis (Nassar and Badr, 1998). Leukotrienes, the products generated by the 5-lipoxygenase pathway, are a family of lipid mediators involved in the pathogenesis of inflammation and allergy. Leukotrienes increase microvascular permeability and are potent chemotactic agents (Wallace et al., 1989). Cysteinyl leukotrienes, namely leukotriene (LT) C4, LTD4 and LTE4, are secreted mainly by eosinophils, mast cells, monocytes and macrophages, and they exert a variety of actions which emphasize their importance as pathogenic elements in the inflammatory states (Damon et al., 1983, Williams et al., 1984). LTs have been detected in serum, urine and renal tissue during glomerular inflammation (Lianos, 1988, Lianos and Noble, 1989, Yared et al., 1991, Petric and Ford-Hutchinson, 1994). The potent chemotactic LTB4 and cysteinyl leukotrienes are suspected of playing an important role in the outcome of pyelonephritis (Tardif et al., 1994). In addition, LTB4 has also been shown to stimulate cell influx in experimental postischemic renal injury (Klausner et al., 1989). Anti-leukotriene agents, i.e. leukotriene receptor antagonists and synthesis inhibitors, have been shown to be effective in several inflammatory models in rats, such as in ethanol-induced gastric mucosal damage (Wallace et al., 1988, Peskar, 1991), colitis (Holma et al., 2001), burn- and sepsis-induced multiorgan damage (Sener et al., 2005a, Sener et al., 2005b) and renal ischemia/reperfusion injury (Sener et al., 2006). Moreover, the selective LTD4 receptor antagonist, montelukast (MK-0476), was used to reduce eosinophilic inflammation in the airways of asthmatic patients (Aharony, 1998, O'Byrne, 1998). Based on these findings, in the present study, the putative protective effect of montelukast against E. coli-induced pyelonephritis was examined using both biochemical and histopathological approaches, while the functional impairments were monitored by renal function tests.