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Effect of human monoclonal antibody against O-antigen and core-antigen of lipopolysaccharide on gut-derived Pseudomonas aeruginosa sepsis in mice



Effect of human monoclonal antibody against O-antigen and core-antigen of lipopolysaccharide on gut-derived Pseudomonas aeruginosa sepsis in mice



Abstracts of the Interscience Conference on Antimicrobial Agents and Chemotherapy 43: 66



Background: Antibiotic therapy against Pseudomonas aeruginosa is frequently ineffective due to its antimicrobial resistance. Therefore, we evaluated the effect of human monoclonal antibody against O-antigen and core-antigen of lipopolysaccharide on gut derived P. aeruginosa sepsis. Methods: Mice were given a suspension of P. aeruginosa strain PA103 or D4 in their drinking water and simultaneously treated with ampicillin (200 mg/kg) to disrupt the normal bacterial flora. Cyclophosphamide was then administered to induce leukopenia and translocation of the P. aeruginosa that had colonized the gastrointestinal tract, thereby producing gut derived generalized sepsis. Results: In this model, intraperitoneal injection of 200 mug/mouse of human monoclonal antibody against O-antigen (SC 1223) for 5 consecutive days significantly (P<0.05) increased the survival rate compared with mice treated with bovine serum albumin. On the other hand, although administration of antibody against core-antigen (SC 1224) alone failed to provide a significant protection, combined administration of SC 1224 and ceftazidime showed significant protection (P<0.05). Treatment with SC 1223 or SC 1224 significantly increased bacterial opsonophagocytosis by cultured murine peritoneal macrophages. Furthermore, administration of SC 1223 significantly decreased tumor necrosis factor (TNF)-alpha release from murine peritoneal macrophages with in vitro stimulation of heat-killed P. aeruginosa. Conclusions: Our results indicate that human monoclonal antibody against O-antigen and core-antigen of lipopolysaccharide protects mice against gut-derived sepsis caused by P. aeruginosa and suggest that such effect may be due to its opsonophagocytic activity and reduced release of TNF-alpha from macrophages.

Accession: 034797451

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