Bacterial Information	Value
Taxonomy level	Species
NCBI Taxonomy ID	1702221
Phylum	Firmicutes
Family	Erysipelotrichaceae
Genus	Faecalibaculum
Gram stain	Gram-positive
Oxygen requirements	Strictly anaerobic
Spore-forming	No
Motile	No
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• Faecalibaculum rodentium
  • Table of Contents
  • Overview
  • Biological information
    • Tumourigenesis
    • Dietary Fat
    • Intestinal epithelial homeostasis

There is only a single recognised species belonging to this genus is Faecalibaculum rodentium. Its human homolog is Holdemanella bioformis.

Anti-proliferative effect on tumour cells via secreted products, e.g. butyrate.

F. rodentium and its human homolog H. bioformis are strongly underrepresented during tumorigenesis (Zagato 2020). It is associated with the mucus of the small and large intestines, but drastically reduced from an early timepoint in mucus from Apc^Min/+ mice (a colorectal cancer (CRC) model). Mucus modification in Apc^Min/+ mice creates an unfavourable environment for F. rodentium colonisation, and oral administration of this bacteria has antitumour effects only following tumour development. F. rodentium was observed to increase faecal SCFAs (propionate, butyrate, and acetate) and reduce lactate, but didn’t alter succinate and isovalerate levels. Alone, or in cooperation with other bacteria, it may affect tumour cell proliferation via the release of SCFAs by inhibiting HDACs and blocking NFATc3 (nuclear factor of activated T cells c3 – a transcription factor important for cell proliferation) and calcineurin (an enzyme that activates T cells) activation. Importantly, supernatant from F. rodentium cultures was alone capable of anti-proliferative activity in vivo – butyrate itself was capable of a similar response.

Decreased in high-fat diets.

Decreased Faecalibaculum has been observed following an isocaloric high-fat diet (20% carbohydrate, 20% protein, 60% fat) for 14 weeks compared to a low-fat, high-carbohydrate diet (70% carbohydrate, 20% protein, 10% fat), however fibre was also increased in the high-fat diet (67g/kg vs. 48g/kg)(Wang 2020).

Involvement in a retinoic acid-eosinophil-interferon-gamma-dependent circuit modulates duodenal epithelial homeostasis

Using single-cell RNA sequencing of duodenal IECs under germ-free (GF) and different conventional microbiota compositions, it was shown that specific microbiota members including F. rodentium alter epithelial homeostasis by increasing epithelial turnover rate, crypt proliferation, and major histocompatibility complex class II (MHCII) expression. F. rodentium decreases enterocyte expression of retinoic-acid-producing enzymes Adh1, Aldh1a1, and Rdh7, reducing retinoic acid signaling required to maintain certain intestinal eosinophil populations. Eosinophils suppress intraepithelial-lymphocyte-mediated production of interferon-γ that regulates epithelial cell function. The authors describe this as a retinoic acid-eosinophil-interferon-γ-dependent circuit by which the microbiota is able to modulate duodenal epithelial homeostasis (Cao 2022).