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A recent publication from the Powrie group at the Kennedy Institute of Rheumatology has described a novel mechanism by which the commensal pathogen Heliobacter hepaticus maintains its niche in the intestinal environment.

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The work, led by Dr Camille Danne in Prof Fiona Powrie’s group, describes the effects of a newly described H. hepaticus secreted polysaccharide on intestinal macrophages, promoting a pro-repair and anti-inflammatory gene signature and effector phenotype.  

The discovery of this mechanism provides a better understanding of the potential means of molecular crosstalk between key host cells in the gut and commensal bacteria.  By further understanding the pathways that promote tolerance and normal homeostasis, these same pathways can potentially be enhanced in order to restore balance after disruptive challenges and interventions such as antibiotic treatment, stress and food allergy, as well as to re-establish a balanced host–microbe dialogue in chronic inflammation.

The study, carried out in collaboration with Prof Simon Arthur’s group in the University of Dundee, was published in Cell Host and Microbe earlier this month and can be accessed here, as was a commentary on the paper from the Kullberg lab which can be found here

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