Inhibition of α2,6-sialyltransferase relieves symptoms of ulcerative colitis by regulating Th17 cells polarization.

Ulcerative colitis (UC) is a chronic, relapsing inflammatory disease that affects human intestines. Immune imbalance is one of the important factors inducing UC. After the activation of CD4 T cells, pro-inflammatory cytokines are produced to induce colonic inflammation.

Hyper α2,6-Sialylation Promotes CD4 T-Cell Activation and Induces the Occurrence of Ulcerative Colitis.

α2,6-sialylation, catalyzed by α2,6-sialyltransferase (ST6GAL1), plays a pivotal role in immune responses. However, the role of ST6GAL1 in the pathogenesis of ulcerative colitis (UC) remains unknown. ST6GAL1 mRNA is highly expressed in UC tissues compared with the corresponding adjacent normal tissues, and α2,6-sialylation is significantly increased in the colon tissues of patients with UC.

Lactobacillus spp. create a protective micro-ecological environment through regulating the core fucosylation of vaginal epithelial cells against cervical cancer.

Vaginal dysbiosis often occurs in patients with cervical cancer. The fucosylation of mucosal epithelial cells is closely related to microbial colonization, and play an important role in protecting the vaginal mucosal epithelial cells. However, no reports on the relationship between vaginal dysbiosis and abnormal mucosal epithelial cell fucosylation, and their roles in the occurrence and development of cervical cancer are unavailable.