Balancing Innate Immunity and Inflammatory State via Modulation of Neutrophil Function: A Novel Strategy to Fight Sepsis

J Immunol Res. 2015:2015:187048. doi: 10.1155/2015/187048. Epub 2015 Dec 21.

Abstract

Sepsis and SIRS (systemic inflammatory response syndrome) belong to a severe disease complex characterized by infection and/or a whole-body inflammatory state. There is a growing body of evidence that neutrophils are actively involved in sepsis and are responsible for both release of cytokines and phagocytosis of pathogens. The neutrophil level is mainly regulated by G-CSF, a cytokine and drug, which is widely used in the septic patient with neutropenia. This review will briefly summarize the role of neutrophils and the therapeutic effect of G-CSF in sepsis. We further suggest that targeting neutrophil function to modulate the balance between innate immunity and inflammatory injury could be a worthwhile therapeutic strategy for sepsis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Acute-Phase Proteins / antagonists & inhibitors
  • Acute-Phase Proteins / genetics
  • Acute-Phase Proteins / immunology
  • Animals
  • Carrier Proteins / antagonists & inhibitors
  • Carrier Proteins / genetics
  • Carrier Proteins / immunology
  • Disease Models, Animal
  • Gene Expression Regulation
  • Granulocyte Colony-Stimulating Factor / genetics
  • Granulocyte Colony-Stimulating Factor / immunology
  • Granulocyte Colony-Stimulating Factor / therapeutic use*
  • Humans
  • Immunity, Innate / drug effects*
  • Membrane Glycoproteins / antagonists & inhibitors
  • Membrane Glycoproteins / genetics
  • Membrane Glycoproteins / immunology
  • Mice
  • NF-kappa B / genetics
  • NF-kappa B / immunology
  • Neutrophils / drug effects*
  • Neutrophils / immunology
  • Neutrophils / pathology
  • Phagocytosis / drug effects
  • Sepsis / drug therapy*
  • Sepsis / genetics
  • Sepsis / immunology
  • Sepsis / pathology
  • Systemic Inflammatory Response Syndrome / drug therapy*
  • Systemic Inflammatory Response Syndrome / genetics
  • Systemic Inflammatory Response Syndrome / immunology
  • Systemic Inflammatory Response Syndrome / pathology
  • Toll-Like Receptor 4 / genetics
  • Toll-Like Receptor 4 / immunology
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / immunology

Substances

  • Acute-Phase Proteins
  • Carrier Proteins
  • Membrane Glycoproteins
  • NF-kappa B
  • TLR4 protein, human
  • Toll-Like Receptor 4
  • Tumor Necrosis Factor-alpha
  • lipopolysaccharide-binding protein
  • Granulocyte Colony-Stimulating Factor