Cross feeding of glucose metabolism byproducts of Escherichia coli human gut isolates and probiotic strains affect survival of Vibrio cholerae.

Vibrio cholerae converts glucose into either acid or the neutral end product acetoin and its survival in carbohydrate enriched media is linked to the nature of the byproducts produced. It has been demonstrated in this study that Escherichia coli strain isolated from the gut of healthy human volunteers and the commonly used probiotic E. coli Nissle strain that metabolize glucose to acidic byproducts drastically reduce the survival of V. cholerae strains irrespective of their glucose sensitivity and acetoin production status. Accordingly, E. coli glucose transport mutants that produce lower amounts of acidic metabolites had little effect on the survival of V. cholerae in cocultures. Thus, cross feeding of byproducts of glucose metabolism by heterologous bacteria modulates the survival of V. cholerae in glucose rich medium suggesting that composition of the gut microbiota could influence the outcome of V. cholerae infection especially when glucose based ORS is administered.

Adherence to Intestinal Cells Promotes Biofilm Formation in Vibrio cholerae.

Vibrio cholerae, the etiological agent of cholera, is known to form biofilms to persist in the environment. It is demonstrated here that even during infection, biofilm genes are upregulated, and microscopic observation indicated that biofilm formation is initiated almost immediately after adherence of V. cholerae to intestinal cells. About 7-fold upregulation of the biofilm regulatory gene vpsT was observed within 30 minutes of adherence of V. cholerae to the intestinal cell line INT 407, and a massive induction of about 700-fold was observed in rabbit ileal loops. The upregulation was observed in the classical and El Tor biotype strains of serogroup O1 that is most frequently associated with epidemic cholera. vpsT upregulation was primarily dependent on the virulence master regulator AphA. Of possible clinical relevance was the observation that V. cholerae in the INT 407-associated biofilms was significantly more resistant to antibiotics than unadhered planktonic cells.

WITHDRAWN: Novel role of LeuO in HNS mediated silencing of the Vibrio cholerae virulence regulatory gene toxT.

This manuscript has been withdrawn by the author.

Fine tuning of virulence regulatory pathways in enteric bacteria in response to varying bile and oxygen concentrations in the gastrointestinal tract.

After entering the gastrointestinal (GI) tract on the way to their physiological site of infection, enteric bacteria encounter a remarkable diversity in environmental conditions. There are gross differences in the physico-chemical parameters in different sections of the GI tract e.g. between the stomach, small intestine and large intestine. Furthermore, even within a certain anatomical site, there are subtle differences in the microenvironment e.g. between the lumen, mucous layer and epithelial surface. Enteric pathogens must not only survive passage through the rapidly changing environments encountered at different niches of the GI tract but must also appropriately coordinate expression of virulence determinants in response to environmental cues at different stages of infection. There are some common themes in the responses of enteric pathogens to environmental cues, there are also distinct differences that may reflect differences in basic pathogenesis mechanisms. The role of bile and oxygen concentration in spatiotemporal regulation of virulence genes in selected enteric pathogens has been reviewed.