Abstract
Actions of endotoxin (1ipopolysaccharide, LPS) in vivo have long been suggested to be mediated by arachidonate metabolites (1,2). The important role of arachidonate-derived metabolites including leukotrienes, prostaglandins and thromboxane in experimental LPS shock has been deduced from the LPS resistance of essential fatty acid-deficient rats (3,4), from the altered arachidonate metabolism in LPS-tolerant rats (5), as well as from pharmacological evidence (1,2,6,7). Recent studies showed that the LPS-resistant C3H/HeJ mouse strain, whose macrophages are defective in prostaglandin (8,9) and leukotriene synthesis (10), can be made highly LPS-sensitive by transfer of pure macrophages from LPS-sensitive C3H/HeN mice (11). These data stress the target cell role of macrophages in the in vivo action of LPS (8,11).
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© 1987 Plenum Press, New York
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Hagmann, W., Denzlinger, C., Rapp, S., Keppler, D. (1987). Leukotrienes in Endotoxin Shock. In: Paubert-Braquet, M., Braquet, P., Demling, B., Fletcher, J.R., Foegh, M. (eds) Lipid Mediators in the Immunology of Shock. NATO ASI Series, vol 139. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0919-2_16
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DOI: https://doi.org/10.1007/978-1-4613-0919-2_16
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