Relative Contribution of ColV Plasmid and K1 Antigen to the Pathogenicity of Escherichia coli

Abstract

The relevance of the ColV plasmid and the capsular K1 antigen in the pathogenicity of E. coli was studied with isogenic strains that differ only in these characteristics. The presence of the ColV plasmid increased the serum resistance of E. coli. This increase did not depend on the expression on the K1 antigen. The presence of the K1 antigen protected E. coli from the bactericidal activity of serum. Studies using mouse peritoneal macrophages in the presence of normal serum indicated that the presence of K1 antigen protects E. coli from phagocytosis. Similar experiments with the K1+ strains performed in the presence of anti-K1 antibodies demonstrated that these antibodies opsonized these bacteria very efficiently in the absence of complement. The K1- E. coli variants were efficiently phagocytized in the presence of normal human serum and absorbed human serum, indicating that they can be opsonized by complement deposited by activation of the alternative complement pathway. Work using fluorescence microscopy confirmed that the K1- strains fix complement in the absence of antibody. The presence of the ColV plasmid may interfere with phagocytosis of the E. coli K1 strains and deposition of complement on these cells. To test the relevance of the results of the in vitro experiments for disease, the pathogenicity of the strains was tested in mice. Apparently, the K1 antigen is the main determinant of pathogenicity of these strains; the presence of ColV can modify the pathogenic potential of the E. coli K1 strains through a mechanism that does not depend on the production of colicin V.