Turicibacter sanguinis - mucosal-immunology-lab/bacterial-database GitHub Wiki
| Bacterial Information | Value |
|---|---|
| Taxonomy level | Species |
| NCBI Taxonomy ID | 154288 |
| Phylum | Firmicutes |
| Family | Turicibacteraceae |
| Genus | Turicibacter |
| Gram stain | Gram-positive |
| Oxygen requirements | Aerotolerant anaerobic or microaerophilic |
| Spore-forming | No |
| Motile | No |
| Image |  |
These are Gram-positive, long, irregular rod-shaped, chain-forming cells, 0.5 – 2.0 x 0.7 – 7.0 μm, and non-spore-forming. Colonies are greyish white with a convex elevation, but irregular form with spreading, undulating margins.
T. sanguinis are chemo-organotrophic, strictly anaerobic, and with fermentative metabolism. Growth is observed at 25 – 46°C (optimum, 37°C) and pH 6.5 – 8.0 (optimum, 7.5).
Catalase and oxidase are negative. Maltose and 5-ketogluconate are the only carbohydrates utilised. Activities for α-glucosidase, α- and β-galactosidase are detected. Nitrates are not reduced. Indole is not produced. Lactate is the main fermentation product. The major cellular fatty acids are C16:0 (37%), C18:0 (15.5%), and C18:1ω9c (14.5%). The DNA has a G+C content of 36.9 mol%. Phylogenetic analysis reveals low relatedness to other bacteria (<88% 16S rDNA similarity).
Serotonin (5-hydroxytryptamine; 5-HT) released from host enterochromaffin cells interacts with Turicibacter in the intestinal lumen via a novel serotonin sensor, CUW_0748, which has homology to the serotonin transporter (SERT) expressed on host enterocytes (Hoffman 2020)(Fung 2019).
Culture experiments showed that T. sanguinis was capable of serotonin uptake and, further, that this effect was inhibited by the selective serotonin reuptake inhibitor (SSRI) fluoxetine (Fung 2019). Heterologous expression of this protein that does not normally express it revealed low levels of serotonin uptake, suggesting additional machinery may be required, or that the protein failed to express correctly. Under conditions of increased serotonin availability in the mouse intestine, enhanced serotonin detection by T. sanguinis leads to increased colonisation (partially inhibited by SSRI activity), alterations in host bacterial community structure, and subsequent changes in steroid and lipid metabolism (Hoffman 2020).
Collectively, these data could have important implications for antidepressant use. A human twin study found a correlation between exposure to the SSRI class of antidepressants and decreased abundance of faecal Turicibacter (Jackson 2018). As altered abundance of Turicibacter has been shown in mouse models of depression and obesity (Jung 2016), it is possible that Turicibacter plays a role in the host anti-depressive effects of SSRIs and/or their adverse effects (e.g., weight gain through altered lipid homeostasis, metabolic syndrome and/or altered gastrointestinal motility).