Immune protection against septic peritonitis in endotoxin-primed mice is related to reduced neutrophil apoptosis

Carolin Feterowski, Heike Weighardt, Klaus Emmanuilidis, Thomas Hartung, Bernhard Holzmann

Research output: Contribution to journalArticlepeer-review

51 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)1268-1277
Number of pages10
JournalEuropean Journal of Immunology
Issue number4
StatePublished - 2001
Externally publishedYes


  • Apoptosis
  • Host defense
  • LPS priming
  • Neutrophils
  • Sepsis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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