Cytokine priming of the respiratory burst in human eosinophils is Ca2+ independent and accompanied by induction of tyrosine kinase activity
We report that pretreatment of human eosinophils with GM‐CSF, IL‐3, or IL‐5 enhanced the respiratory burst induced by opsonized particles. In order to gain more insight into the intracellular mechanism(s) involved in cytokine priming, the role of [Ca2+], and tyrosine kinases was studied. Optimal pri...
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Published in | Journal of leukocyte biology Vol. 53; no. 4; pp. 347 - 353 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Bethesda, MD
Society for Leukocyte Biology
01.04.1993
Federation of American Societies for Experimental Biology |
Subjects | |
Online Access | Get full text |
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Summary: | We report that pretreatment of human eosinophils with GM‐CSF, IL‐3, or IL‐5 enhanced the respiratory burst induced by opsonized particles. In order to gain more insight into the intracellular mechanism(s) involved in cytokine priming, the role of [Ca2+], and tyrosine kinases was studied. Optimal priming concentrations of GM‐CSF, IL‐3, and IL‐5 did not induce a rise in [Ca2+]i, and Ca2+‐depleted eosinophils ([Ca2+]i < 20 nM) were still primed after preincubation with these cytokines. GM‐CSF, IL‐3, and IL‐5 induced phosphorylation of two proteins (102 and 122 kd) on tyrosine residues, as deduced from Western blot analysis with an antiphospho‐ tyrosine monoclonal antibody (4G10). This cytokine‐ stimulated tyrosine phosphorylation was not inhibited under Ca2+‐depleted conditions. In conclusion, this study demonstrates that GM‐CSF, IL‐3, and IL‐5 priming of the opsonized particle‐induced respiratory burst in human eosinophils is completely Ca2+ independent. Moreover the tyrosine phosphorylation of a 102‐kd and a 122‐kd protein is Ca2+ independent, suggesting that this event might be involved in cytokine priming. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0741-5400 1938-3673 |
DOI: | 10.1002/jlb.53.4.347 |