作者: Catherine H. Valentine , Judith Hellman , Laura K. Beasley-Topliffe , Aranya Bagchi , H. Shaw Warren
DOI: 10.2119/2006-00065.VALENTINE
关键词:
摘要: Multiple older studies report that immunoglobulin directed to rough mutant bacteria, such as E. coli J5, provides broad protection against challenge with heterologous strains of Gram-negative bacteria. This was initially believed occur through binding bacterial lipopolysaccharide (LPS). However, hundreds millions dollars have been invested in attempting develop clinically-effective anti-LPS monoclonal antibodies without success, and no study has shown IgG from this antiserum binds LPS. Identification the protective mechanism would facilitate development broadly human for treating sepsis. 2 outer membrane proteins: murein lipoprotein (MLP) peptidoglycan-associated (PAL). Both these proteins are highly conserved, lipid domains anchored membrane, shed bacteria blebs together LPS, activate cells Tolllike receptor 2. Our goal current work determine if passive immunization MLP PAL protects mice Neither nor polyclonal or conferred survival 3 different models sepsis: cecal ligation puncture, an infected burn model, fibrin clot model mimicking peritonitis. results not supportive hypothesis either anti-MLP anti-PAL previously described anti-rough antisera. These suggest a is involved.