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Human S100A9 potentiates IL‐8 production in response to GM‐CSF or fMLP via activation of a different set of transcription factors in neutrophils
Author(s) -
Simard Jean-Christophe,
Noël Claudie,
Tessier Philippe A.,
Girard Denis
Publication year - 2014
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2014.04.027
Subject(s) - creb , activator (genetics) , cytokine , stat3 , stat5 , transcription factor , chemistry , proinflammatory cytokine , stat protein , microbiology and biotechnology , inflammation , immunology , biology , signal transduction , biochemistry , receptor , gene
Inflammation is highly regulated by various agents. Unexpectedly, we report here that the damage‐associated molecular pattern S100A9 protein, a potent neutrophil activator and inducer of cytokine production in monocytes, is not a direct activator of cytokine production in human neutrophils. However, S100A9 primed IL‐8 production in fMLP‐ and GM‐CSF‐stimulated neutrophiles via NF‐κB and CREB‐1, and NF‐κB, STAT3 and STAT5, respectively. Pharmacological inhibition confirmed the importance of these transcription factors by significantly decreasing IL‐8 production. This is the first time that a different set of transcription factors are shown to be involved in S100A9‐primed neutrophils in response to proinflammatory agonist.