R-Spondin 2 signalling mediates susceptibility to fatal infectious diarrhoea

Olivier Papapietro, Sarah Teatero, Ajitha Thanabalasuriar, Kyoko E. Yuki, Eduardo Diez, Lei Zhu, Eugene Kang, Sandeep Dhillon, Aleixo M. Muise, Yves Durocher, Martin M. Marcinkiewicz, Danielle Malo and Samantha Gruenheid ()
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Olivier Papapietro: McGill University
Sarah Teatero: McGill University
Ajitha Thanabalasuriar: McGill University
Kyoko E. Yuki: Complex Traits Program, McGill University
Eduardo Diez: McGill University
Lei Zhu: McGill University
Eugene Kang: McGill University
Sandeep Dhillon: SickKids Inflammatory Bowel Disease Center and Cell Biology Program, Research Institute, Hospital for Sick Children
Aleixo M. Muise: SickKids Inflammatory Bowel Disease Center and Cell Biology Program, Research Institute, Hospital for Sick Children
Yves Durocher: Biotechnology Research Institute, National Research Council of Canada
Martin M. Marcinkiewicz: Cytochem Inc.
Danielle Malo: Complex Traits Program, McGill University
Samantha Gruenheid: McGill University

Nature Communications, 2013, vol. 4, issue 1, 1-9

Abstract: Abstract Citrobacter rodentium is a natural mouse pathogen widely used as a model for enteropathogenic and enterohemorrhagic Escherichia coli infections in humans. While C. rodentium causes self-limiting colitis in most inbred mouse strains, it induces fatal diarrhoea in susceptible strains. The physiological pathways as well as the genetic determinants leading to susceptibility have remained largely uncharacterized. Here we use a forward genetic approach to identify the R-spondin2 gene as a major determinant of susceptibility to C. rodentium infection. Robust induction of R-spondin2 expression during infection in susceptible mouse strains causes a potent Wnt-mediated proliferative response of colonic crypt cells, leading to the generation of an immature and poorly differentiated colonic epithelium with deficiencies in ion-transport components. Our data demonstrate a previously unknown role of R-spondins and Wnt signalling in susceptibility to infectious diarrhoea and identify R-spondin2 as a key molecular link between infection and intestinal homoeostasis.

Date: 2013
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DOI: 10.1038/ncomms2816

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