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Escherichia coli F-18 makes a streptomycin-treated mouse large intestine colonization factor when grown in nutrient
P S Cohen1, S Kjelleberg, D C Laux
1Department of Microbiology, University of Rhode Island, Kingston 02881.
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.
Insights
Glucose triggers Escherichia coli F-18 FimA- to clump and settle, impacting its colonization of the mouse gut. This glucose-induced settling, linked to catabolite repression, is crucial for E. coli gut colonization.
Area of Science:
- Microbiology
- Bacterial Physiology
- Gastrointestinal Health
Background:
- Escherichia coli F-18 FimA- colonizes streptomycin-treated mouse intestines similarly to its parent strain.
- Type 1 fimbriae are not essential for this colonization process.
Purpose of the Study:
- To investigate the role of glucose in the behavior of E. coli F-18 FimA-.
- To determine the impact of glucose-induced changes on bacterial colonization.
Main Methods:
- Culturing E. coli F-18 FimA- in nutrient broth with and without glucose.
- Supplementing glucose media with cyclic AMP to observe reversal effects.
- Selecting and testing a reduced-settling mutant (E. coli F-18 FimA- Set-) for colonization ability.
Main Results:
- Glucose induced E. coli F-18 FimA- to form clumps (microcolonies) and settle in liquid culture.
- Cyclic AMP partially reversed the glucose-induced settling.
- A mutant with reduced settling ability was a poor colonizer in vivo.
Conclusions:
- Glucose-induced settling in E. coli F-18 FimA- is likely regulated by catabolite repression.
- Microcolony formation, influenced by glucose, is important for E. coli gut colonization in streptomycin-treated mice.