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Modulation of leukotriene B4 and platelet-activating factor binding to neutrophils

Modulation of leukotriene B4 and platelet-activating factor binding to neutrophils YAMAZAKI, THADDEUS F. P. MOLSKI, TIMOTHY STEVENS, HUANG, ELMER L. BECKER, RAMADAN I. SHA’AFI University Connecticut Health Center, Departments Physiology Pathology, Farmington, Connecticut 06032 YAMAZAKI, MUNEHIRO, THADDEUS F. P. MOLSKI, TIMOTHY STEVENS, CHI-KUANG HUANG, ELMER L. BECKER, RAMADAN I. SHA’AFI. Modulation leukotriene B4 plateletactivating factor to neutrophils. Am. J. Physiol. 261 (Cell Physiol. 30): CW%C520,1991.-Preincubation human neutrophils with the human hormone granulocyte-macrophage colony-stimulating factor (GM-CSF) inhibits the specific leukotriene B4 ( [3H]LTB4) but not the nonmetabolizable bioactive platelet-activating factor ( [3H]C-) to intact cells. This inhibition requiresthat the GM-CSF interacts with intact cells. The action GM-CSF is not prevented by pertussis toxin. Moreover, the rise in calcium produced by but not by is also inhibited in human neutrophils pretreated with GM-CSF. Interestingly, neither the inhibitory action GMCSF on [3H]LTB4 or LTB4-induced calcium rise nor the potentiation superoxide production by GM-CSF is reduced by inhibitors arachidonic acid metabolism by the lipoxygenase pathway. In contrast, preincubation human neutrophils with either the chemotactic factor formyl-methionyl-leucyl-phenylalanine (fMet-Leu-Phe) or the active phorbol ester, phorbol 12-myristate 13-acetate (PMA), inhibits the both [3H]LTBq [3H]C- to intact cells. The inhibitory actions GM-CSF, PMA, fMet-Leu-Phe require that they interact with the intact cells; their actions cannot be http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Cell Physiology The American Physiological Society

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