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Postnatal development of the small intestinal mucosa drives age-dependent, regio-selective susceptibility to Escherichia coli K1 infection

Journal article
Authors George M. H. Birchenough
F. Dalgakiran
L. A. Witcomb
Malin E V Johansson
A. J. McCarthy
Gunnar C. Hansson
P. W. Taylor
Published in Scientific Reports
Volume 7
ISSN 2045-2322
Publication year 2017
Published at Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Language en
Links doi.org/10.1038/s41598-017-00123-w
Keywords paneth cells, necrotizing enterocolitis, gene-expression, mouse stomach, mucus layers, rats, colonization, newborn, mice, macropinocytosis, Science & Technology - Other Topics
Subject categories Microbiology in the medical area, Biochemistry and Molecular Biology

Abstract

The strong age dependency of neonatal systemic infection with Escherichia coli K1 can be replicated in the neonatal rat. Gastrointestinal (GI) colonization of two-day-old (P2) rats leads to invasion of the blood within 48 h of initiation of colonization; pups become progressively less susceptible to infection over the P2-P9 period. We show that, in animals colonized at P2 but not at P9, E. coli K1 bacteria gain access to the enterocyte surface in the mid-region of the small intestine and translocate through the epithelial cell monolayer by an intracellular pathway to the submucosa. In this region of the GI tract, the protective mucus barrier is poorly developed but matures to full thickness over P2-P9, coincident with the development of resistance to invasion. At P9, E. coli K1 bacteria are physically separated from villi by the mucus layer and their numbers controlled by mucus-embedded antimicrobial peptides, preventing invasion of host tissues.

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