Pathogenesis of intraabdominal abscess formation: abscess-potentiating agents and inhibition of complement-dependent opsonization of abscess-inducing bacteria
Related Experiment Videos
J J Finlay-Jones1, P A Kenny, M F Nulsen
1Department of Microbiology and Infectious Diseases, School of Medicine, Flinders University of South Australia, Adelaide.
Abstract:
Bacteroides fragilis and Escherichia coli are synergistic in the production of intraabdominal abscesses. However, these bacteria initiate abscess formation only when inoculated with an agent such as autoclaved colonic contents (ACC) or bran (a fiber analogue). The mechanism of action of the abscess-potentiating agent was studied. Opsonins in normal mouse serum were determined for phagocytic killing by murine neutrophils of B. fragilis and E. coli. Opsonization required fixation of complement by the alternative pathway. ACC (0.2 mg/ml) and bran (1.0 mg/ml) inhibited phagocytic killing of Proteus mirabilis in the presence of normal but not immune serum. Assay of the alternative pathway of complement activation indicated that both bacterial components and abscess-potentiating agents in an abscess-inducing mixture activated complement. These findings suggest that abscess-potentiating agents inhibit opsonization and therefore the subsequent phagocytic killing of bacteria in the nonimmune host.
Insights
Abscess-potentiating agents, like autoclaved colonic contents (ACC), hinder the immune system's ability to engulf bacteria. This inhibition of opsonization allows bacteria like Bacteroides fragilis and Escherichia coli to cause intraabdominal abscesses.
Area of Science:
- Microbiology
- Immunology
- Pathogenesis
Background:
- Bacteroides fragilis and Escherichia coli are key players in intraabdominal abscess formation.
- Abscess development requires bacterial synergy and an abscess-potentiating agent, such as autoclaved colonic contents (ACC) or bran.
- The precise mechanism by which these agents facilitate abscess formation remains unclear.
Purpose of the Study:
- To investigate the mechanism of action of abscess-potentiating agents in bacterial abscess formation.
- To determine how autoclaved colonic contents (ACC) and bran influence the interaction between bacteria and the host immune system.
- To elucidate the role of complement and phagocytosis in abscess development.
Main Methods:
- Assessing opsonins in normal mouse serum for phagocytic killing of B. fragilis and E. coli by murine neutrophils.
- Investigating the requirement of complement fixation via the alternative pathway for opsonization.
- Evaluating the impact of ACC and bran on the phagocytic killing of Proteus mirabilis in normal and immune serum.
- Assaying the alternative pathway of complement activation in the presence of bacterial components and abscess-potentiating agents.
Main Results:
- Opsonization of B. fragilis and E. coli for phagocytic killing by neutrophils necessitates complement fixation through the alternative pathway.
- Abscess-potentiating agents, specifically ACC (0.2 mg/ml) and bran (1.0 mg/ml), significantly inhibited the phagocytic killing of Proteus mirabilis in normal serum.
- This inhibition by ACC and bran was not observed in immune serum, suggesting a targeted effect on non-specific host defenses.
- Both bacterial components and abscess-potentiating agents were found to activate complement via the alternative pathway when present in an abscess-inducing mixture.
Conclusions:
- Abscess-potentiating agents, such as ACC and bran, interfere with the opsonization process.
- This interference with opsonization subsequently impairs the phagocytic killing of bacteria by neutrophils in a non-immune host.
- These findings highlight a critical mechanism by which commensal bacteria can transition to pathogens, leading to abscess formation.