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. 2017 Jan 19;117(1):93–107. doi: 10.1017/S0007114516004037

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© The Authors 2017

This is an Open Access article, distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives licence (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. The written permission of Cambridge University Press must be obtained for commercial re-use or in order to create a derivative work.

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Fig. 1 — Direct and indirect mechanisms by which commensals or probiotics can antagonise pathogens. Graphical display of exemplary direct (a) and indirect (b) mechanisms of barrier function modulation by bacterial (probiotic) interaction. (a) Direct mechanisms of barrier function modulation by interaction of commensals and probiotics. Bacteria can compete with enteric pathogens by competition for carbohydrates depending on the diet⁽ ²²⁷ ⁾. A probiotic strain of Lactobacillus salivarius UCC118 produces a bacteriocin in vivo that can significantly protect mice against infection with the invasive foodborne pathogen Listeria monocytogenes ⁽ ³⁶ ⁾. In diverse Bacteroides species, a type VI secretion system (T6SS) mediates cell-contact-dependent mechanisms of inter-bacterial antagonism via the export antibacterial proteins⁽ ²²⁸ ⁾. Probiotics have been shown to inhibit the colonisation of pathogens through competition for common receptors of adhesion⁽ ⁴⁸ ⁾. (b) Indirect mechanisms of pathogen antagonism. Recognition of microbe-associated molecular patterns by host pattern recognition receptors such as TLR and NLR activate immune defences and protect against infection. TLR signalling induces expression of defensins in enterocytes and antimicrobial factors in Paneth cells via the myeloid differentiation primary response 88 (MYD88) activation of NF-κB leading to the production of antimicrobial peptides. Similarly, nucleotide-binding oligomerisation domain 2 (NOD2) recognition of bacterial peptidoglycan induces cryptdin expression by Paneth cells. Sensing of an unknown signal from commensal microbes stimulates type 3 innate lymphoid cells (ILC) to secrete IL-22, which signals through the receptor (IL-22R) on intestinal epithelial cells to increase expression of the fucosyltransferase (FUT), mucin expression and antimicrobials, including regenerating family member 3 (Reg3) proteins. Segmented filamentous bacteria (SFB) closely associate with the ileum epithelium and stimulate maturation of the B- and T-cell compartments leading to enhanced IgA production by B cells and serum amyloid A (SAA)-dependent T helper 17 (Th17) cell differentiation. Th17 cells produce inflammatory cytokines and IL-22, which stimulate innate immune defence mechanisms to fight off infections.