Colicins and T6SS-based competition systems enhance enterotoxigenic E. coli (ETEC) competitiveness

ABSTRACT

Diarrheal diseases are still a significant problem for humankind, causing approximately half a million deaths annually. To cause diarrhea, enteric bacterial pathogens must first colonize the gut, which is a niche occupied by the normal bacterial microbiota. Therefore, the ability of pathogenic bacteria to inhibit the growth of other bacteria can facilitate the colonization process. Although enterotoxigenic Escherichia coli (ETEC) is one of the major causative agents of diarrheal diseases, little is known about the competition systems found in and used by ETEC and how they contribute to the ability of ETEC to colonize a host. Here, we collected a set of 94 fully assembled ETEC genomes by performing whole-genome sequencing and mining the NCBI RefSeq database. Using this set, we performed a comprehensive search for delivered bacterial toxins and investigated how these toxins contribute to ETEC competitiveness in vitro. We found that type VI secretion systems (T6SS) were widespread among ETEC (n = 47). In addition, several closely related ETEC strains were found to encode Colicin Ia and T6SS (n = 8). These toxins provide ETEC competitive advantages during in vitro competition against other E. coli, suggesting that the role of T6SS as well as colicins in ETEC biology has until now been underappreciated.

Keywords:

• ETEC
• colicin
• type VI secretion
• competitive advantage
• genome

Disclosure statement

No potential conflict of interest was reported by the author(s).

Author contributions

J. K., D. L., R. D., O. B. V., and S. K. performed experiments. J.K, D.L, H.S, R.D and S.K analyzed data. J. K., D. L., H. S., R. D., O. B. V., K. H., and S. K. wrote the manuscript.

Data availability statement

All raw data for the manuscript are freely available either as supplementary excel files (Tables S5–8) or at the NCBI Reference Sequence Database (GCF_032367395.1, GCF_032365155.1, GCF_032366635.1, GCF_032368225.1).

Supplementary material

Supplemental data for this article can be accessed online at https://doi.org/10.1080/19490976.2023.2295891.

Additional information

Funding

This work was partly supported by grants from the ERC and the Swedish Research Council (to S. K.), Sven and Lily Lawski Foundation (to D. L.), and partly by the University of Bergen and the Research Council of Norway (to K. H.).