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The effect of inhibition of leukotriene synthesis on the activity of interleukin‐8 and granulocyte‐macrophage colony‐stimulating factor
Author(s) -
Pamela Roberts,
Arnold Pizzey,
David C. Linch
Publication year - 1993
Publication title -
mediators of inflammation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.37
H-Index - 97
eISSN - 1466-1861
pISSN - 0962-9351
DOI - 10.1155/s0962935193000286
Subject(s) - leukotriene b4 , leukotriene , granulocyte , superoxide , interleukin , granulocyte macrophage colony stimulating factor , priming (agriculture) , chemistry , integrin alpha m , extracellular , leukotriene c4 , interleukin 3 , immunology , pharmacology , cytokine , biology , inflammation , biochemistry , immune system , enzyme , t cell , antigen presenting cell , asthma , botany , germination
The cytokines interleukin-8 (IL-8) and granulocyte-macrophage colony-stimulating factor (GM-CSF) enhanced the extracellular release of arachidonate metabolites from ionophore-stimulated neutrophils by 145 +/- 10% (mean +/- S.E.M., n = 13) and 182 +/- 11% (n = 16), respectively. To determine whether enhanced leukotriene production mediates the effects of these cytokines on neutrophil activity, two different specific arachidonate 5-lipoxygenase (5-LO) inhibitors, piriprost and MK-886, were used to inhibit leukotriene synthesis. Neither inhibitor affected the upregulation of CD11b beta(2)-integrin expression or priming of superoxide generation stimulated by IL-8 and GM-CSF. It is concluded that leukotrienes do not mediate either the direct or priming effects of these cytokines and that these classes of anti-inflammatory drugs are therefore unlikely to inhibit the effects of IL-8 and GM-CSF on neutrophil activation.

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