Bacteroides thetaiotaomicron and Faecalibacterium prausnitzii influence the production of mucus glycans and the development of goblet cells in the colonic epithelium of a gnotobiotic model rodent
By Laura Wrzosek, S. Miquel, Marie‐Louise Noordine, S. Bouet, Marie Joncquel Chevalier-Curt, V. Robert, C. Philippe, C. Bridonneau, C. Cherbuy, C. Robbe-Masselot and 2 more. BMC Biology, 2013
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The intestinal mucus layer plays a key role in the maintenance of host-microbiota homeostasis. To document the crosstalk between the host and microbiota, we used gnotobiotic models to study the influence of two major commensal bacteria, Bacteroides thetaiotaomicron and Faecalibacterium prausnitzii, on this intestinal mucus layer. B. thetaiotaomicron is known to use polysaccharides from mucus, but its effect on goblet cells has not been addressed so far. F. prausnitzii is of particular physiological importance because it can be considered as a sensor and a marker of human health. We determined whether B. thetaiotaomicron affected goblet cell differentiation, mucin synthesis and glycosylation in the colonic epithelium. We then investigated how F. prausnitzii influenced the colonic epithelial responses to B. thetaiotaomicron. B. thetaiotaomicron, an acetate producer, increased goblet cell differentiation, expression of mucus-related genes and the ratio of sialylated to sulfated mucins in mono-associated rats. B. thetaiotaomicron, therefore, stimulates the secretory lineage, favoring mucus production. When B. thetaiotaomicron was associated with F. prausnitzii, an acetate consumer and a butyrate producer, the effects on goblet cells and mucin glycosylation were diminished. F. prausnitzii, by attenuating the effects of B. thetaiotaomicron on mucus, may help the epithelium to maintain appropriate proportions of different cell types of the secretory lineage. Using a mucus-producing cell line, we showed that acetate up-regulated KLF4, a transcription factor involved in goblet cell differentiation. B. thetaiotaomicron and F. prausnitzii, which are metabolically complementary, modulate, in vivo, the intestinal mucus barrier by modifying goblet cells and mucin glycosylation. Our study reveals the importance of the balance between two main commensal bacteria in maintaining colonic epithelial homeostasis via their respective effects on mucus.
Subfields: Food Science, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/a8f59e563cd762cf30b16c3307b7efb958e40c84
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In Food Science
In Molecular Biology
- G. Núñez
- Bernard Henrissat
- D. Ríos-Covian
- P. Ruas-Madiedo
- C. G. de los Reyes-Gavilán
- Harry Sokol
- N. Salazar
- Vincent B. Young
Citations in the corpus
- Intestinal Short Chain Fatty Acids and their Link with Diet and Human Health (2016, background): “…Salazar nuriasg@ipla.csic.es Specialty section: This article was submitted to Microbial Physiology and Metabolism, a section of the journal Frontiers in Microbiology Received: 04 December 2015 Accepted: 02 February 2016 Published: 17 February 2016 Citation: Ríos-Covián D, Ruas-Madiedo P,”
- Identification of an anti-inflammatory protein from Faecalibacterium prausnitzii, a commensal bacterium deficient in Crohn's disease (2015, background): “prausnitzii on intestinal homeostasis and during an acute colitis [19] [20].”
- Faecalibacterium prausnitzii and human intestinal health. (2013, background): “prausnitzii that it could influence gut physiology through mucus pathway and the production of mucus O-glycans [16 ].”
- A dietary fiber-deprived gut microbiota degrades the colonic mucus barrier and enhances pathogen susceptibility (2016, positive): “(Petersson et al., 2011; Wrzosek et al., 2013), which found that microbial colonization or exposure to cues such as peptidoglycan or lipopolysaccharides is required for mucus production.”
- Intestinal barrier and gut microbiota: Shaping our immune responses throughout life (2017, background): “prausnitzii induced goblet cell differentiation and mucus production.(27) In vitro, intestinal epithelial goblet cells increased their transcription of mucin genes in response to SCFAs.”