This finding points to an easily administered and inexpensive approach where commensal bacteria are engineered to communicate with invasive species and potentially prevent human disease.
impact statement issue
impact statement response
To investigate the possibility of using commensal bacteria as signal mediators for inhibiting the disease cholera (caused by infection with the marine bacterium V. cholerae), we stably transformed commensal bacteria to express the autoinducer molecule CAI-1 (shown previously to prevent virulence when present with another signaling molecule, AI-2 at high concentrations) and determined the effect on V. cholerae virulence gene expression and infectivity in an infant mouse model. We found that pretreatment of mice for eight hours with commensal bacteria engineered to express CAI-1 (Nissle-cqsA) greatly increased the mice’s survival (92 percent) from ingestion of V. cholerae. Pretreatment with Nissle-cqsA for only four hours increased survival by 77 percent, while ingesting Nissle-cqsA at the same time as V. cholerae increased survival rates by 27 percent. Immuno-staining revealed an 80 percent reduction in cholera toxin binding to the intestines of mice pretreated for eight hours with Nissle-cqsA. Further, the numbers of V. cholerae in treated mouse intestines was reduced by 69 percent after 40 hours.
impact statement summary
By transforming commensal bacteria, we were able to inhibit the progression of cholera in mice.
