Abstract
To study the relevance of the ColV plasmid and the capsular K1 antigen in the pathogenicity of Escherichia coli, isogenic strains that differ only in these characteristics were constructed. Studies with these variants demonstrated that the presence of the ColV plasmid increased the serum resistance of E. coli. This increase did not depend on the expression of the K1 antigen. This work also demonstrated that the presence of the K1 antigen protects 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 are able to be opsonized by complement deposited by activation of the alternative pathway of complement. Work using fluorescence microscopy confirmed that the K1(-) strains are able to fix complement in the absence of antibody. It was also found that 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. The results showed that the K1 antigen is the main determinant of pathogenicity of these strains and that 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.