Abstract
Escherichia coli F-18 FimA-, a type 1 fimbria-less derivative of a normal human fecal isolate, E. coli F-18, has previously been shown to be as good a colonizer of streptomycin-treated mouse large intestine as its parent, suggesting that type 1 fimbriae are not necessary in this process. In this study it was found that when E. coli F-18 FimA- was grown standing overnight at 37 degrees C in nutrient broth, it remained uniformly suspended; however, when grown in nutrient broth containing 1% (wt/wt) D-glucose, it settled to the bottom of culture tubes. Settling was associated with the formation of clumps (microcolonies) of more than 10 cells each. The effect of glucose could be partially reversed by growing E. coli F-18 FimA- in nutrient broth containing 1% D-glucose supplemented with cyclic AMP (greater than or equal to 1 mM). A reduced-settling mutant of E. coli F-18 FimA-, E. coli F-18 FimA- Set-, selected after Tn5 mutagenesis, was found to be a poor colonizer of streptomycin-treated mouse large intestine when fed to mice simultaneously with the parent strain. These results suggest that glucose-induced settling is, at least in part, regulated in a way related to catabolite repression and that the ability of E. coli F-18 FimA- to form microcolonies plays an important role in its ability to colonize streptomycin-treated mouse large intestine.
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Selected References
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