Adhesion promotes transcellular leukotriene biosynthesis during neutrophil-glomerular endothelial cell interactions: Inhibition by antibodies against CD18 and L-selectin

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Summary

Eicosanoid formation by transcellular routes can amplify the levels and types of lipid mediators within a local milieu. To evaluate the role of adhesion in this process, we assessed the influence of mAb against adhesion molecules on LTC4 generation by PMN-endothelial cell interaction. Transcellular LTC4 generation was initiated by addition of fMLP to coincubations of GM-CSFprimed PMN and TNF-activated endothelial cells cultured from kidney glomeruli. Both PMN-endothelial cell adhesion and transcellular LTC4 generation were inhibited by mAb against leukocyte L-selectin and CD18. These results indicate that cytokine-treated PMN and endothelial cells generate LTC4 via transcellular routes by receptor-triggered mechanisms. They suggest that adhesion promotes transcellular eicosanoid biosynthesis and that adhesion molecules may also be targets for blockade of transcellular biosynthesis of lipid mediators.

References (17)

  • SamuelssonB. et al.

    Science Wash. DC

    (1987)
  • ClaessonH-E et al.

    Eur. J. Biochem.

    (1988)
  • FeinmarkS.J. et al.

    J. Biol. Chem.

    (1988)
  • FeinmarkS.J. et al.

    Adv. Prost. Thromb. Leuk. Res.

    (1989)
  • EdeniusC. et al.

    Eur. J. Biochem.

    (1988)
  • FioreS. et al.

    J. Exp. Med.

    (1990)
  • SpringerT.A.

    Nature

    (1990)
  • PoberJ.S. et al.

    Physiol. Rev.

    (1990)
There are more references available in the full text version of this article.

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