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      Production of Indole-3-Lactic Acid by Bifidobacterium Strains Isolated fromHuman Infants

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          Abstract

          Recent studies have shown that metabolites produced by microbes can be considered as mediators of host-microbial interactions. In this study, we examined the production of tryptophan metabolites by Bifidobacterium strains found in the gastrointestinal tracts of humans and other animals. Indole-3-lactic acid (ILA) was the only tryptophan metabolite produced in bifidobacteria culture supernatants. No others, including indole-3-propionic acid, indole-3-acetic acid, and indole-3-aldehyde, were produced. Strains of bifidobacterial species commonly isolated from the intestines of human infants, such as Bifidobacterium longum subsp. longum, Bifidobacterium longum subsp. infantis, Bifidobacterium breve, and Bifidobacterium bifidum, produced higher levels of ILA than did strains of other species. These results imply that infant-type bifidobacteria might play a specific role in host–microbial cross-talk by producing ILA in human infants.

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          Symbiotic bacterial metabolites regulate gastrointestinal barrier function via the xenobiotic sensor PXR and Toll-like receptor 4.

          Madhukumar Venkatesh, Subhajit Mukherjee, Hongwei Wang … (2014)
          Intestinal microbial metabolites are conjectured to affect mucosal integrity through an incompletely characterized mechanism. Here we showed that microbial-specific indoles regulated intestinal barrier function through the xenobiotic sensor, pregnane X receptor (PXR). Indole 3-propionic acid (IPA), in the context of indole, is a ligand for PXR in vivo, and IPA downregulated enterocyte TNF-α while it upregulated junctional protein-coding mRNAs. PXR-deficient (Nr1i2(-/-)) mice showed a distinctly "leaky" gut physiology coupled with upregulation of the Toll-like receptor (TLR) signaling pathway. These defects in the epithelial barrier were corrected in Nr1i2(-/-)Tlr4(-/-) mice. Our results demonstrate that a direct chemical communication between the intestinal symbionts and PXR regulates mucosal integrity through a pathway that involves luminal sensing and signaling by TLR4.
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            Bifidobacteria and Their Role as Members of the Human Gut Microbiota

            Amy O'Callaghan, Douwe van Sinderen (2016)
            Members of the genus Bifidobacterium are among the first microbes to colonize the human gastrointestinal tract and are believed to exert positive health benefits on their host. Due to their purported health-promoting properties, bifidobacteria have been incorporated into many functional foods as active ingredients. Bifidobacteria naturally occur in a range of ecological niches that are either directly or indirectly connected to the animal gastrointestinal tract, such as the human oral cavity, the insect gut and sewage. To be able to survive in these particular ecological niches, bifidobacteria must possess specific adaptations to be competitive. Determination of genome sequences has revealed genetic attributes that may explain bifidobacterial ecological fitness, such as metabolic abilities, evasion of the host adaptive immune system and colonization of the host through specific appendages. However, genetic modification is crucial toward fully elucidating the mechanisms by which bifidobacteria exert their adaptive abilities and beneficial properties. In this review we provide an up to date summary of the general features of bifidobacteria, whilst paying particular attention to the metabolic abilities of this species. We also describe methods that have allowed successful genetic manipulation of bifidobacteria.
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              Lactobacillus reuteri induces gut intraepithelial CD4 + CD8αα + T cells

              Victor S. Cortez, Luisa Cervantes-Barragan, Jiani N Chai … (2017)
              The small intestine contains CD4+CD8αα+ double-positive intraepithelial T lymphocytes (DP IELs), which originate from intestinal CD4+ T cells through downregulation of the transcription factor ThPOK and have regulatory functions. DP IELs are absent in germ-free mice, suggesting that their differentiation depends on microbial factors. We found that DP IEL numbers in mice varied in different vivaria, correlating with the presence of Lactobacillus reuteri. This species induced DP IELs in germ-free mice and conventionally raised mice lacking these cells. L. reuteri did not shape DP–IEL–TCR repertoire, but generated indole derivatives of tryptophan that activated the aryl-hydrocarbon receptor in CD4+ T cells, allowing ThPOK downregulation and differentiation into DP IELs. Thus, L. reuteri together with a tryptophan-rich diet can reprogram intraepithelial CD4+ T cells into immunoregulatory T cells.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Microorganisms
                Journal ID (iso-abbrev): Microorganisms
                Journal ID (publisher-id): microorganisms
                Title: Microorganisms
                Publisher: MDPI
                ISSN (Electronic): 2076-2607
                Publication date (Electronic): 11 September 2019
                Publication date Collection: September 2019
                Volume: 7
                Issue: 9
                Electronic Location Identifier: 340
                Affiliations
                Next Generation Science Institute, Morinaga Milk Industry Co., Ltd., Zama, Kanagawa 252-8583, Japan; t_sakura@ 123456morinagamilk.co.jp (T.S.); t-odamak@ 123456morinagamilk.co.jp (T.O.)
                Author notes
                [* ]Correspondence: j_xiao@ 123456morinagamilk.co.jp ; Tel.: +81-46(252)3068; Fax: +81-46(252)3077
                Author information
                https://orcid.org/0000-0001-6019-9240
                https://orcid.org/0000-0002-8512-9086
                Article
                Publisher ID: microorganisms-07-00340
                DOI: 10.3390/microorganisms7090340
                PMC ID: 6780619
                PubMed ID: 31514325
                SO-VID: 10a6e080-d79d-4322-b18d-5df79ba1392b
                Copyright © © 2019 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 29 July 2019
                Date accepted : 09 September 2019
                Categories
                Subject: Communication

                Keywords: bifidobacterium,indole-3-lactic acid,indole-3-propionic acid,indole-3-acetic acid,indole-3-aldehyde
                Data availability:
                Keywords: bifidobacterium, indole-3-lactic acid, indole-3-propionic acid, indole-3-acetic acid, indole-3-aldehyde

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