2. Academic Validation
  3. Human S100A9 potentiates IL-8 production in response to GM-CSF or fMLP via activation of a different set of transcription factors in neutrophils

Human S100A9 potentiates IL-8 production in response to GM-CSF or fMLP via activation of a different set of transcription factors in neutrophils

  • FEBS Lett. 2014 Jun 13;588(13):2141-6. doi: 10.1016/j.febslet.2014.04.027.
Jean-Christophe Simard 1,  Claudie Noël 1,  Philippe A Tessier 2,  Denis Girard 3
Affiliations

Affiliations

  • 1 Laboratoire de Recherche en Inflammation et Physiologie des Granulocytes, Université du Québec, Canada.
  • 2 Axe Maladies Infectieuses et Immunitaires, Centre de Recherche du CHU de Québec, and Faculté de Médecine, Université Laval, Québec, Canada.
  • 3 Laboratoire de Recherche en Inflammation et Physiologie des Granulocytes, Université du Québec, Canada. Electronic address: Denis.girard@iaf.inrs.ca.
PMID: 24796790 DOI: 10.1016/j.febslet.2014.04.027
Abstract

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.

Keywords

CREB-1; NF-κB; Neutrophil; S100A9; STAT-3; STAT-5.

Figures
Products