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Oral tolerance failure upon neonatal gut colonization with Escherichia coli producing the genotoxin colibactin. | LitMetric

Oral tolerance failure upon neonatal gut colonization with Escherichia coli producing the genotoxin colibactin.

Infect Immun

INRA, USC 1360, Toulouse, France INSERM, UMR 1043, Toulouse, France CNRS, UMR 5282, Toulouse, France Université de Toulouse, UPS, Centre de Physiopathologie Toulouse Purpan, Toulouse, France CHU Toulouse, Hôpital Purpan, Service de Bactériologie-Hygiène, Toulouse, France

Published: June 2015

AI Article Synopsis

Article Abstract

The intestinal barrier controls the balance between tolerance and immunity to luminal antigens. When this finely tuned equilibrium is deregulated, inflammatory disorders can occur. There is a concomitant increase, in urban populations of developed countries, of immune-mediated diseases along with a shift in Escherichia coli population from the declining phylogenetic group A to the newly dominant group B2, including commensal strains producing a genotoxin called colibactin that massively colonized the gut of neonates. Here, we showed that mother-to-offspring early gut colonization by colibactin-producing E. coli impairs intestinal permeability and enhances the transepithelial passage of luminal antigen, leading to an increased immune activation. Functionally, this was accompanied by a dramatic increase in local and systemic immune responses against a fed antigen, decreased regulatory T cell population, tolerogenic dendritic cells, and enhanced mucosal delayed-type hypersensitivity response. Conversely, the abolition of colibactin expression by mutagenesis abrogates the alteration of oral tolerance induced by neonatal colonization by E. coli. In conclusion, the vertical colonization by E. coli producing the genotoxin colibactin enhances intestinal translocation and subsequently alters oral tolerance. Thus, early colonization by E. coli from the newly dominant phylogenetic group B2, which produces colibactin, may represent a risk factor for the development of immune-mediated diseases.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4432747PMC
http://dx.doi.org/10.1128/IAI.00064-15DOI Listing

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