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Real friends: Faecalibacterium prausnitzii supports mucosal immune homeostasis
  1. Mathias W Hornef1,
  2. Oliver Pabst2
  1. 1Institute of Medical Microbiology, RWTH University Hospital, Aachen, Germany
  2. 2Institute of Molecular Medicine, RWTH University Hospital, Aachen, Germany
  1. Correspondence to Professor Mathias W Hornef, Institute of Medical Microbiology, RWTH University Hospital, Pauwelsstr. 30, Aachen 52074, Germany; mhornef{at}ukaachen.de

https://doi.org/10.1136/gutjnl-2015-310027

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    IBD is commonly considered as an exaggerated immune response to the microbiota in a genetically susceptible host. This statement recognises the central role of the enteric microbiota in the pathogenesis of IBD. Consistently, in animal models of IBD, inflammation is not observed in the absence of live bacteria and distinct members of the microbiota differ in their potential to trigger disease. Patients with IBD present substantial changes of their microbiota commonly described as dysbiosis.1–4 However, intestinal bacteria not only drive disease but quite the contrary, individual commensal members also dampen inflammatory responses and might thereby contribute to maintain host–microbial homeostasis (figure 1). This aspect seems of particular interest since it may provide the opportunity to develop therapeutic anti-inflammatory strategies.

    Figure 1

    Immunomodulatory effects of the microbiota and specific commensal bacteria. Tryptophan metabolites via the aryl hydrocarbon receptor (AhR) modulate intraepithelial lymphocytes (IELs) and stimulate RAR-related orphan receptor ((ROR)γt+) type 3 innate lymphocytes (ILCs) to promote cryptopatch and isolated lymphoid follicles (ILFs) as well as interleukin 22 (IL-22) secretion. IL-22 in turn stimulates the expression of the antibacterial c-type lectin Reg3γ. Also, short-chain fatty acids (SCFAs) resulting from bacterial degradation of dietary fibres induce the expression of an antimicrobial peptide, the cathelicidin LL37. SCFAs additionally activate the G-coupled protein receptors 43 and 109a inducing K+ release and stimulation of the inflammasome leading to barrier reinforcement. SCFAs also induce differentiation and proliferation of T regulatory (TREG) cells. Examples of specific effects are the microbial anti-inflammatory molecules (MAM) secreted from Faecalibacterium prausnitzii that inhibit cellular NF-κB signalling and inflammation. Polysaccharide A (PSA) produced by Bacteroides fragilis stimulates via Toll-like receptor (TLR)2 interleukin 10 (IL-10) secretion and the differentiation of TREG cells. Lactocepin released …

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    Footnotes

    • Contributors MWH and OP contributed equally to write the manuscript.

    • Funding Deutsche Forschungsgemeinschaft. MWH is supported by the German Research Foundation (DFG Ho2236/8-1), the DFG Priority Programs SPP1580 and SSP1565, the Collaborative Research Center SFB900, as well as the Niedersachsen-Research Network on Neuroinfectiology (N-RENNT) and the German Israel Collaborative Initiative (11-76251-99-10/12).

    • Competing interests None declared.

    • Provenance and peer review Commissioned; internally peer reviewed.

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