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Review
. 2024 Jan-Dec;16(1):2379624.
doi: 10.1080/19490976.2024.2379624. Epub 2024 Jul 23.

Mechanisms of intestinal dysbiosis: new insights into tuft cell functions

Affiliations
Review

Mechanisms of intestinal dysbiosis: new insights into tuft cell functions

Nathalie Coutry et al. Gut Microbes. 2024 Jan-Dec.

Abstract

Symbiosis between the host and intestinal microbial communities is essential for human health. Disruption in this symbiosis is linked to gastrointestinal diseases, including inflammatory bowel diseases, as well as extra-gastrointestinal diseases. Unbalanced gut microbiome or gut dysbiosis contributes in multiple ways to disease frequency, severity and progression. Microbiome taxonomic profiling and metabolomics approaches greatly improved our understanding of gut dysbiosis features; however, the precise mechanisms involved in gut dysbiosis establishment still need to be clarified. The aim of this review is to present new actors and mechanisms underlying gut dysbiosis formation following parasitic infection or in a context of altered Paneth cells, revealing the existence of a critical crosstalk between Paneth and tuft cells to control microbiome composition.

Keywords: Gut microbiome; Paneth cell; RegIII; dysbiosis; succinate; tuft cell; type 2 immunity.

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Conflict of interest statement

No potential conflict of interest was reported by the author(s).

Figures

Figure 1.
Figure 1.
Tuft cell-induced intestinal epithelium remodeling and AMP shifts leading to microbiota reshaping following tuft cell activation by microbial-derived succinate.
Figure 2.
Figure 2.
Multi-step mechanism responsible for gut dysbiosis and inflammation establishment following a crosstalk between altered Paneth cells and tuft cells, involving a succinate-SuncR1 axis and type 2 cytokines.

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References

    1. MetaHIT Consortium, Qin J, Li R, Raes J, Arumugam M, Burgdorf KS, Manichanh C, Nielsen T, Pons N, Levenez F, et al. A human gut microbial gene catalogue established by metagenomic sequencing. Nature. 2010;464(7285):59–18. doi:10.1038/nature08821. - DOI - PMC - PubMed
    1. Postler TS, Ghosh S.. Understanding the holobiont: how microbial metabolites affect human health and shape the immune system. Cell Metab. 2017;26(1):110–130. doi:10.1016/j.cmet.2017.05.008. - DOI - PMC - PubMed
    1. Tremaroli V, Bäckhed F. Functional interactions between the gut microbiota and host metabolism. Nature. 2012;489(7415):242–249. doi:10.1038/nature11552. - DOI - PubMed
    1. Thaiss CA, Zmora N, Levy M, Elinav E. The microbiome and innate immunity. Nature. 2016;535(7610):65–74. doi:10.1038/nature18847. - DOI - PubMed
    1. Leone V, Gibbons SM, Martinez K, Hutchison AL, Huang EY, Cham CM, Pierre JF, Heneghan AF, Nadimpalli A, Hubert N, et al. Effects of diurnal variation of gut microbes and high-fat feeding on host circadian clock function and metabolism. Cell Host & Microbe. 2015;17(5):681–689. doi:10.1016/j.chom.2015.03.006. - DOI - PMC - PubMed

Publication types

Grants and funding

This work was supported by Agence Nationale de la Recherche [ANR-14-CE14-0025-01 and ANR-17-CE15-0016-01 to P.J.], Institut National du Cancer [INCa 2014-174 to P.J. and INCA_2018-158 to P.J.], Fondation ARC [ARCPGA12021020003077_3570], Ligue Nationale contre le Cancer [Equipe labellisée], and SIRIC Montpellier Cancer [grant INCa_Inserm_DGOS_12553 to P.J.].

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