title: Immune protection against septic peritonitis in endotoxin-primed mice is related to reduced neutrophil apoptosis.
abstract: The innate immune system provides essential information about the presence of infectious danger and signals the activation and instruction of adaptive immunity. The present study addressed the question of whether prior exposure of the innate immune system to LPS may modulate host defense against acute septic peritonitis. We show that LPS priming 4 days, but not 2 days, prior to infection enhances bacterial clearance and improves survival of septic peritonitis. Immune protection in day 4 LPS-primed mice was specifically associated with a marked increase in the accumulation and activation of neutrophils at the site of infection. Accumulating neutrophils in day 4 LPS-primed mice exhibited a normal production of reactive oxygen metabolites in response to in vivo exposure to intestinal bacteria. The local increase in neutrophil numbers was found to result from a reduced rate of apoptotic cell death. Inhibition of neutrophil apoptosis in LPS-primed mice was mediated by soluble factor(s) distinct from G-CSF and GM-CSF. Thus, engagement of pattern recognition systems prior to infection may improve host defense by amplifying the effector cell response of innate immunity. The results also provide in vivo evidence that apoptosis of inflammatory cells represents an important process for the control of host defense to infection.
authors: Department of Surgery, Klinikum rechts der Isar, Technische Universität München, München, Germany.
authors: C
authors: C
authors: Feterowski
authors: H
authors: H
authors: Weighardt
authors: K
authors: K
authors: Emmanuilidis
authors: T
authors: T
authors: Hartung
authors: B
authors: B
authors: Holzmann
mesh_terms: D000818:Animals; D017209:Apoptosis; D001424:Bacterial Infections / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D002448:Cell Adhesion; D002470:Cell Survival; D018925:Chemokines / Q000276:immunology; D003106:Colon / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D016207:Cytokines / Q000097:blood / Q000378:metabolism; D005260:Female; D005434:Flow Cytometry; D007113:Immunity, Innate / Q000276:immunology; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D008070:Lipopolysaccharides / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018375:Neutrophil Activation / Q000276:immunology; D009504:Neutrophils / Q000166:cytology / Q000276:immunology* / Q000473:pathology*; D010529:Peritoneal Cavity / Q000382:microbiology / Q000473:pathology; D010533:Peritoneal Lavage; D010538:Peritonitis / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D017382:Reactive Oxygen Species / Q000378:metabolism; D018805:Sepsis / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D015996:Survival Rate; D013997:Time Factors
chemical_list: D018925:Chemokines; D016207:Cytokines; D008070:Lipopolysaccharides; D017382:Reactive Oxygen Species