| First Author | Coletto E | Year | 2023 |
| Journal | Sci Rep | Volume | 13 |
| Issue | 1 | Pages | 13982 |
| PubMed ID | 37634035 | Mgi Jnum | J:339673 |
| Mgi Id | MGI:7523691 | Doi | 10.1038/s41598-023-40497-8 |
| Citation | Coletto E, et al. (2023) Role of mucin glycosylation in the gut microbiota-brain axis of core 3 O-glycan deficient mice. Sci Rep 13(1):13982 |
| abstractText | Alterations in intestinal mucin glycosylation have been associated with increased intestinal permeability and sensitivity to inflammation and infection. Here, we used mice lacking core 3-derived O-glycans (C3GnT(-/-)) to investigate the effect of impaired mucin glycosylation in the gut-brain axis. C3GnT(-/-) mice showed altered microbial metabolites in the caecum associated with brain function such as dimethylglycine and N-acetyl-L-tyrosine profiles as compared to C3GnT(+/+) littermates. In the brain, polysialylated-neural cell adhesion molecule (PSA-NCAM)-positive granule cells showed an aberrant phenotype in the dentate gyrus of C3GnT(-/-) mice. This was accompanied by a trend towards decreased expression levels of PSA as well as ZO-1 and occludin as compared to C3GnT(+/+). Behavioural studies showed a decrease in the recognition memory of C3GnT(-/-) mice as compared to C3GnT(+/+) mice. Combined, these results support the role of mucin O-glycosylation in the gut in potentially influencing brain function which may be facilitated by the passage of microbial metabolites through an impaired gut barrier. |
