The molecular basis for control of ETEC enterotoxin expression in response to environment and host
Research output: Contribution to journal › Article
Colleges, School and Institutes
Diarrheagenic illness remains a major disease burden in the developing world. Enterotoxigenic Escherichia coli (ETEC) are the leading bacterial cause of such disease; hundreds of millions of cases occur every year. The severe watery diarrhoea associated with ETEC infections results from the action of enterotoxins. The toxins target human gut epithelial cells and trigger the loss of water and electrolytes into the gut lumen. Oral rehydration therapy can counteract this process. Hence, glucose and salt solutions promote rehydration of the patient. In this work we show that the gene regulatory mechanisms controlling toxin expression respond directly to sugar and salt. Furthermore, we describe a molecular mechanism to explain these effects. Hence, we provide a starting point for the optimisation of oral rehydration solutions to reduce toxin expression over the course of an ETEC infection.
|Publication status||Published - 8 Jan 2015|
- Glucose, Sequence motif analysis, Toxins, Gene targeting, Gene regulation, DNA transcription, Gene expression, Escherichia coli infections