Diarrhea is the second leading cause of mortality of children under the age of 5 in developing countries with Enteropathogenic E. coli (EPEC) and Vibrio cholerae as the two main pathogens that cause infantile diarrhea. The two pathogens have a common infection site, the small intestine, and they both utilize a specialized transport complex, called type III secretion system (T3SS), for their ability to infect host cells. The T3SS resembles a nano syringe, which extends from the bacterial membrane to the plasma membrane of the host cell and injects virulence effector proteins into the host cells cytoplasm. In this study, we examined whether EPEC can sense V. cholerae presence and respond to it by modulating its virulence mechanisms. We found that EPEC virulence is enhanced in response to elevated concentrations of the main quorum sensing (QS) molecule of Vibrio cholera, cholera autoinducer-1 (CAI-1), even though neither a CAI-1 synthase nor receptor have been reported in E. coli. This CAI-1 sensing and virulence upregulation response may facilitate the ability of EPEC to coordinate successful colonization of a host when co-infected with V. cholerae. To the best of our knowledge, this is the first observed example of ‘eavesdropping’ between two bacterial pathogens that is based on interspecies sensing of a QS molecule. We recently examined whether addition ofmicrobiota-produced metabolite, found in high levels in the human gut, affect this pathogen cross-talk. Surprisingly, we found that although this metabolite does not affect V. cholerae's growth or CAI-1 production, it inhibits the upregulation of EPEC virulence in the presence of V. cholerae. This QS-based-mechanism may well be a broader phenomenon that occurs in other pathogens that infect common environmental niches, and could presents exciting new research avenue.

Diarrhea is the second leading cause of mortality of children under the age of 5 in developing countries with Enteropathogenic _E. coli_ (EPEC) and _Vibrio_ _cholerae_ as the two main pathogens that cause infantile diarrhea. The two pathogens have a common infection site, the small intestine, and they both utilize a specialized transport complex, called type III secretion system (T3SS), for their ability to infect host cells. The T3SS resembles a nano syringe, which extends from the bacterial membrane to the plasma membrane of the host cell and injects virulence effector proteins into the host cells cytoplasm. In this study, we examined whether EPEC can sense _V. cholerae_ presence and respond to it by modulating its virulence mechanisms. We found that EPEC virulence is enhanced in response to elevated concentrations of the main quorum sensing (QS) molecule of _Vibrio cholera_, cholera autoinducer-1 (CAI-1), even though neither a CAI-1 synthase nor receptor have been reported in _E. coli_. This CAI-1 sensing and virulence upregulation response may facilitate the ability of EPEC to coordinate successful colonization of a host when co-infected with _V. cholerae_. To the best of our knowledge, this is the first observed example of ‘eavesdropping’ between two bacterial pathogens that is based on interspecies sensing of a QS molecule. We recently examined whether addition ofmicrobiota-produced metabolite, found in high levels in the human gut, affect this pathogen cross-talk. Surprisingly, we found that although this metabolite does not affect _V. cholerae's_ growth or CAI-1 production, it inhibits the upregulation of EPEC virulence in the presence of _V. cholerae_. This QS-based-mechanism may well be a broader phenomenon that occurs in other pathogens that infect common environmental niches, and could presents exciting new research avenue.

The effect of extracellular environment moleculles on Enteropathogenic E coli virulence

Exploring the intricacies of host-pathogen communication is vital in order to understand why
some microbes persist within a host, while others are effectively cleared. As such,
host-pathogen communication is an urgent area of research underpinning human health
and disease, especially given the emerging concerns of antibiotic resistance.
Understanding host-pathogen pathways requires intricate knowledge in the fields of both
microbiology and immunology.

Living in a world of specialists, where scientists sometimes invest their whole career
studying one organism, a specific pathway or a protein, multidisciplinary discussions of
host-pathogen interactions are highly needed. This international conference will provide
such a forum for scientific exchange at the highest level, between scientists from different
research areas related to host-pathogen interactions, with the aim to trigger fruitful
collaborations addressing the urgent questions in the field.

This meeting has an additional special focus of bringing researchers from Ireland, Denmark
and Israel together to learn about cutting edge biology and form new collaborations.
Thus, the conference will be a showcase for the exciting and original research emanating
from these three small but innovative countries.

Host-Pathogen Communication (HPC) 2021

Helminths battle type 2 immunity for control of the intestinal stem cell niche