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. 2023 Aug 2;26(9):107515. doi: 10.1016/j.isci.2023.107515

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© 2023 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

PMC Copyright notice

BGN deficiency enhanced IL-10 expression in mouse enteric neurons induced by LPS

(A) Heatmap showing the top 31 DEGS in BGN ^(-/0) and WT control enteric neurons and LPS-treated BGN ^(-/0) and WT mouse enteric neurons.

(B) BGN deficiency reduced the level of IL-10 in AOM/DSS-treated mice, as detected by ELISA assay (n = 7 mice/group).

(C and D) Representative image presenting transwell co-culture of MC38 cells and the enteric neurons from BGN ^(-/0) and WT mice with LPS (100 μg/L). The number of MC38 cells migration was decreased in co-culture with BGN ^(-/0) mice enteric neurons with LPS (100 μg/L) treatment (n = 3 biological replicates/group).

(E and F) Representative image presenting transwell co-culture of MC38 cells and the enteric neurons from BGN ^(-/0) and IL-10 knockdown of BGN ^(-/0) enteric neurons with LPS (100 μg/L). The number of MC38 cells migration was increased in co-culture with IL-10 knockdown of BGN ^(-/0) mice enteric neurons (n = 3 biological replicates/group).

(G and H) BGN deficiency upregulated the IL-10 expression of enteric neurons in CAC mice (n = 4 mice/group).

Data are representative or cumulative results of at least two independent experiments (B–H). Data are presented as mean ± S.E.M. ∗p < 0.05 and ∗∗p < 0.01.