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Berard, M.

Publications and source records attributed to Berard, M..

2 recordsLinked to original sources

Specific targeting of intestinal Prevotella copri by a Listeria monocytogenes bacteriocin

Deciphering the specific function of every microorganism in microbial gut communities is a key issue to interrogate their role during infection. Here, we report the discovery of a Listeria bacteriocin, Lmo2776, that specifically targets the abundant gut commensal Prevotella copri and affects Listeria infection. Oral infection of conventional mice with a {Delta}lmo2776 mutant leads to a thinner intestinal mucus layer and higher Listeria loads both in the intestinal content and deeper tissues compared to WT Listeria, while no difference is observed in germ-free mice. This microbiota-dependent effect is phenocopied by precolonization of germ-free mice before Listeria infection, with P. copri, but not with other commensals. Together, these data unveil a role for Prevotella in controlling intestinal infection, highlighting that pathogens may selectively deplete microbiota to avoid excessive inflammation.

microbiology

Excess calorie intake early in life increases susceptibility to colitis in the adult

Epidemiological data report an association between obesity and inflammatory bowel disease (IBD) 1-3. Furthermore, animal models demonstrate that maternal high fat diet (HFD) and maternal obesity increase susceptibility to IBD in the offsprings 4-8. However, the mechanisms that translate maternal obesity and HFD into increased susceptibility to IBD later in life remain unknown. Here we report that excess calorie intake by neonatal mice, as a consequence of maternal HFD, forced feeding of neonates or low litter competition, lead to an increase, during weaning, in intestinal permeability, expression of pro-inflammatory cytokines and hydrogen sulfide production by the microbiota. In this context, intestinal permeability, cytokine expression and hydrogen sulfide engaged in a mutual positive feedback that imprinted increased susceptibility to colitis in the adult. This pathological imprinting was prevented by the neutralization of IFN{gamma} and TNF, of the production of hydrogen sulphide, or by normalization of intestinal permeability during weaning. Thus, excessive calorie intake by neonates leads to multiple causally-linked perturbations in the intestine that imprint the individual with long term susceptibility to IBD.

immunology