Altered inflammatory responses in leukotriene-deficient mice.
Copyright policy )Altered inflammatory responses in leukotriene-deficient mice.
Leukotrienes have been implicated in the regulation of immune responses, including inflammation and immediate hypersensitivity reactions. Here, we describe the phenotypic analysis of leukotriene-deficient mice generated by inactivation of the 5-lipoxygenase (5LO) gene. These 5LO(-/-) mice were unable to synthesize detectable levels of leukotrienes and were more resistant to lethal anaphylaxis induced by platelet-activating factor. The intensity of an acute inflammatory response induced by arachidonic acid was similar in 5LO(-/-) mice and controls. However, the response in 5LO(-/-) mice, but not in controls, could be virtually eliminated by a cyclooxygenase inhibitor. These data suggest that inflammatory responses are modulated by arachidonic acid metabolites through a variety of interconnected mechanisms. This has important implications for understanding the early events of an inflammatory response and for designing drugs for use in therapeutic intervention.
- Duke University United States
- University of North Carolina at Chapel Hill United States
Inflammation, Mice, Knockout, Leukotrienes, Arachidonate 5-Lipoxygenase, Neutrophils, Macrophages, Dinoprostone, Leukotriene C4, Thromboxane B2, Chemotaxis, Leukocyte, Mice, Animals, Edema, Platelet Activating Factor, Anaphylaxis
Inflammation, Mice, Knockout, Leukotrienes, Arachidonate 5-Lipoxygenase, Neutrophils, Macrophages, Dinoprostone, Leukotriene C4, Thromboxane B2, Chemotaxis, Leukocyte, Mice, Animals, Edema, Platelet Activating Factor, Anaphylaxis
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