In:
International Archives of Allergy and Immunology, S. Karger AG, Vol. 131, No. Suppl. 1 ( 2003), p. 15-19
Abstract:
〈 i 〉 Background: 〈 /i 〉 Platelet-activating factor (PAF) is a potent stimulator of eosinophils. Recently, treatment with a protein kinase C (PKC) inhibitor which generally inhibits PKC isoforms has been shown to modulate several eosinophil functions in distinct manners, in that PKC inhibition enhanced CD11b expression and cellular adhesion, but inhibited superoxide generation and degranulation in PAF-stimulated human eosinophils. These results suggested that distinct PKC isoforms were likely to be involved in each eosinophil function induced by PAF. We have therefore investigated whether or not the PKC isoforms involved in PAF-induced CD11b expression and superoxide generation were different. 〈 i 〉 Methods: 〈 /i 〉 Human eosinophils prepared from healthy volunteers were treated with PKC inhibitors, bis-indolylmaleimide I (BisI; a general PKC inhibitor), myristoylated PKC inhibitor peptide (myr-ψPKC; a PKCα, β and δ inhibitor) and rottlerin (a PKCδ inhibitor), followed by stimulation with PAF. CD11b expression was determined using flow cytometry and superoxide generation was evaluated using a cytochrome c reduction assay. 〈 i 〉 Results: 〈 /i 〉 BisI treatment led to enhancement of PAF-induced CD11b expression, while myr-ψPKC and rottlerin did not. In contrast, PAF-induced superoxide generation was inhibited by treatment with BisI, myr-ψPKC and rottlerin. 〈 i 〉 Conclusions: 〈 /i 〉 PKCα, β and δ are not involved in PAF-induced CD11b expression, but PKCδ is involved in the PAF-induced activation of superoxide anion generation.
Type of Medium:
Online Resource
ISSN:
1018-2438
,
1423-0097
Language:
English
Publisher:
S. Karger AG
Publication Date:
2003
detail.hit.zdb_id:
1482722-0
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