Effect of Escherichia coli Lipopolysaccharide on Bacteroides fragilis Abscess Formation and Mortality in Mice

• Published in: MICROBIOLOGY and IMMUNOLOGY Vol. 38; no. 2; pp. 97 - 102
• Main Authors: Tanaka, Yasunori, Jotwani, Ravi, Watanabe, Kunitomo, Tanaka, Kaori, Kato, Naoki, Ueno, Kazue
• Format: Journal Article
• Language: English
• Published: Australia Blackwell Publishing Ltd 01-01-1994; Center For Academic Publications Japan
• Subjects: Abscess - etiology; Abscess - immunology; Animals; Bacteroides fragilis; Bacteroides fragilis - pathogenicity; Bacteroides fragilis abscesses; Bacteroides Infections - etiology; Bacteroides Infections - immunology; Cytokines - biosynthesis; Escherichia coli; Escherichia coli - pathogenicity; lipopolysaccharide (LPS); Lipopolysaccharides - toxicity; Male; Mice; Mice, Inbred C57BL; Mortality; Peritonitis - etiology; Peritonitis - immunology
• ISSN: 0385-5600; 1348-0421
• DOI: 10.1111/j.1348-0421.1994.tb01749.x

To study the mechanism of synergism between Bacteroides fragilis and Escherichia coli, the effect of sublethal dose of E. coli lipopolysaccharide (LPS) (25μg/mouse) was checked on B. fragilis abscess formation. LPS was administered prior or after inoculum injection. No significant difference in the abscess size was observed at necropsy on day 6. However, all the groups receiving LPS showed higher incidence of recovery of additional intestinal bacteria (23.5-45.5%) from the abscess pus. When LPS was given 4hr prior to inoculum administration, 83-100% mortality was observed. Detailed investigation showed autoclaved cecal contents alone could also cause similar mortality. Studies with stimulation of endogenous cytokines by E. coli LPS demonstrated induction of all of them within 3hr in the blood stream with TNF-α demonstrating peak at 1hr, IL-1α and IL-6 at 4hr and IFN-γ between 6-9hr with moderately high levels at 4hr. This E. coli LPS-triggered cytokine cascade possibly gets further stimulated by injection of autoclaved cecal contents containing high concentration of endotoxins (1.6×105EU/ml) contributed by dead bacteria and lead to the mortality of animals.