title: Balancing Innate Immunity and Inflammatory State via Modulation of Neutrophil Function: A Novel Strategy to Fight Sepsis.
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.
authors.affiliation: Department of Pathophysiology, Anhui Medical University, Hefei 230032, China.
authors.forename: Haoshu
authors.initials: H
authors.lastname: Fang
authors.affiliation: Department of Pathophysiology, Anhui Medical University, Hefei 230032, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Jiang
authors.affiliation: Department of Pathophysiology, Anhui Medical University, Hefei 230032, China.
authors.forename: Jin
authors.initials: J
authors.lastname: Cheng
authors.affiliation: Department of Pathophysiology, Anhui Medical University, Hefei 230032, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Lu
authors.affiliation: Experimental Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
authors.forename: Anding
authors.initials: A
authors.lastname: Liu
authors.affiliation: Department of Pathophysiology, Anhui Medical University, Hefei 230032, China; Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
authors.forename: Lixin
authors.initials: L
authors.lastname: Kan
authors.affiliation: Experimental Transplantation Surgery, Department of General, Visceral and Vascular Surgery, Jena University Hospital, 07747 Jena, Germany.
authors.forename: Uta
authors.initials: U
authors.lastname: Dahmen
mesh_terms: D000209:Acute-Phase Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000276:immunology; D000818:Animals; D002352:Carrier Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000276:immunology; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D016179:Granulocyte Colony-Stimulating Factor / Q000235:genetics / Q000276:immunology / Q000627:therapeutic use*; D006801:Humans; D007113:Immunity, Innate / Q000187:drug effects*; D008562:Membrane Glycoproteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000276:immunology; D051379:Mice; D016328:NF-kappa B / Q000235:genetics / Q000276:immunology; D009504:Neutrophils / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D010587:Phagocytosis / Q000187:drug effects; D018805:Sepsis / Q000188:drug therapy* / Q000235:genetics / Q000276:immunology / Q000473:pathology; D018746:Systemic Inflammatory Response Syndrome / Q000188:drug therapy* / Q000235:genetics / Q000276:immunology / Q000473:pathology; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000235:genetics / Q000276:immunology; D000099231:Lipopolysaccharide-Binding Protein
chemical_list: D000209:Acute-Phase Proteins; D002352:Carrier Proteins; D016179:Granulocyte Colony-Stimulating Factor; D008562:Membrane Glycoproteins; D016328:NF-kappa B; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D000099231:Lipopolysaccharide-Binding Protein; C495345:TLR4 protein, human