Lipopolysaccharide desensitization of macrophages provides protection against Yersinia enterocolitica-induced apoptosis.

Abstract

Pathogenic Yersinia spp. uncouple an array of signal transduction pathways in macrophages to disrupt their response to infection. This compels the macrophage to undergo apoptosis. Our study shows that macrophages that had acquired tolerance to Yersinia infection by preexposure to lipopolysaccharide were considerably protected against Y. enterocolitica-induced apoptosis. The desensitization of macrophages by lipopolysaccharide, which is thought to be a self-protective, adaptive response to sustained bacterial stimulation, may represent an immune mechanism that aids in overcoming Yersinia-mediated apoptosis and infection.

• Authors: Klaus Ruckdeschel, Kathleen Richter
• Journal: Infection and immunity (Infect Immun) Vol. 70 Issue 9 Pg. 5259-64 (Sep 2002) ISSN: 0019-9567 [Print] United States
• PMID: 12183578 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Bacterial Proteins
• Lipopolysaccharides
• NF-kappa B
• YopP protein, Yersinia
• DNA

Topics

• Adaptation, Physiological
• Animals
• Apoptosis (drug effects, immunology)
• Bacterial Proteins (immunology)
• Base Sequence
• Binding Sites (genetics)
• Cell Line
• DNA (genetics, metabolism)
• Immune Tolerance
• Lipopolysaccharides (pharmacology)
• Macrophages (drug effects, immunology, microbiology, pathology)
• Mice
• NF-kappa B (metabolism)
• Salmonella typhimurium (pathogenicity)
• Signal Transduction
• Yersinia enterocolitica (immunology, pathogenicity, physiology)