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Effects of interleukin‐13 on human neutrophil functions
Author(s) -
Girard Denis,
Faquin Robert,
Naccache Paul H.,
Beaulieu André D.
Publication year - 1996
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.59.3.412
Subject(s) - biology , cytokine , tyrosine phosphorylation , interleukin 8 , microbiology and biotechnology , receptor , interleukin , phagocytosis , signal transduction , immunology , biochemistry
It was recently shown that interleukin‐13 (IL‐13) induces the expression and release of the IL‐1 decoy receptor (type II) in human neutrophils along with the production of the IL‐1 receptor antagonist. In the present study we focused on further studying the modulatory effects of IL‐13 on these cells. We found that recombinant human IL‐13 (rhIL‐13) induces cellular morphological changes in neutrophils that are typical of activated cells. Furthermore, rhIL‐13 was shown to increase tyrosine phosphorylation of several neutrophil proteins. We also demonstrate that this cytokine stimulates de novo RNA synthesis in a concentration‐dependent fashion as measured by [5‐ 3 H]uridine incorporation and that rhIL‐13 induces the synthesis of several neutrophil proteins according to high‐resolution two‐dimensional gel electrophoresis of metabolically [ 35 S]‐labeled cells. We observed that the IL‐8 levels in the external milieu of IL‐13‐stimulated cells was almost fivefold increased when compared with control cells. Finally, we observed that rhIL‐13 has no significant effect on phagocytosis and apoptosis. Taken together, our results demonstrate that IL‐13 is a modulator of several human neutrophil functions. This leads us to conclude that the modulatory role of IL‐13 on human neutrophils, a potentially important anti‐inflammatory cytokine, is more complex than previously believed. Furthermore, because we show that the synthesis of several as yet unidentified proteins was up‐regulated by IL‐13, our findings open new avenues of research on the effects of this cytokine on human neutrophils.