Conclusion
AKK-OMVs can directly stimulate goblet cells to promote MUC2 secretion, providing potential for further in vivo studies to confirm their protective effects against indomethacin-induced intestinal injury.
Methods
The abnormal mucin secretion model in LS174T cells was established using indomethacin, with treatment including Akkermansia muciniphila (AKK) supernatant, AKK-OMVs, and extracellular vesicle removal supernatant. The effects of these treatment on MUC2 expression were observed. Transcriptomic sequencing analysis was used to explore the underlying regulatory mechanisms, which were further validated through qRT-PCR and western blotting.
Results
The treatment with AKK supernatant and AKK-OMVs alleviated the indomethacin-induced reduction in MUC2 secretion in goblet cells. Mechanistically, transcriptomic analysis showed that the gene expression associated with endoplasmic reticulum (ER) stress were upregulated after indomethacin treatment in LS174T cells. This suggests that AKK-OMVs, as the active component in the supernatant, improved MUC2 expression by inhibiting ER stress.