Article (Scientific journals)
MyD88 Mediates Colitis- and RANKL-Induced Microfold Cell Differentiation
Li, Yang; Yang, Shanshan; Huang, Xin et al.
2021In Veterinary Sciences, 9
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Keywords :
colonic M cells; MyD88; colitis; DSS
Abstract :
[en] Intestinal microfold (M) cells are critical for sampling antigens in the gut and initiating the intestinal mucosal immune response. In this study, we found that the oral administration of dextran sulfate sodium (DSS) and Salmonella infection induced colitis. In the process, the expression levels ofM cell differentiation-related genes were synchronized with the kinetics of pro-inflammatory cytokines. Compared to wild-type (WT) mice, MyD88-/- mice exhibited significantly lower expression levels of M cell differentiation-related genes. However, DSS induced colitis in MyD88-/- mice but failed to promote the transcription of M cell differentiation related genes. Furthermore, the receptor activator of the Nuclear Factor-kB ligand (RANKL) upregulated the transcription of M cell differentiation related genes in murine intestinal organoids prepared from both WT and MyD88-/- mice. Meanwhile, fewer changes in M cell differentiation related genes were found in MyD88-/- mice as compared to WT mice. Hence, we concluded that myeloid differentiation factor 88 (MyD88) is an essential molecule for colitis- and RANKL-related differentiation of M cells.
Disciplines :
Veterinary medicine & animal health
Author, co-author :
Li, Yang
Yang, Shanshan
Huang, Xin
Yang, Ning
Wang, Caiying
Zhao, Jing
Jing, Zhizhong
Willems, Luc  ;  Université de Liège - ULiège > GIGA Cancer - Cellular and Molecular Epigenetics
Liu, Guangliang
Language :
English
Title :
MyD88 Mediates Colitis- and RANKL-Induced Microfold Cell Differentiation
Publication date :
24 December 2021
Journal title :
Veterinary Sciences
eISSN :
2306-7381
Publisher :
MDPI AG, Switzerland
Volume :
9
Peer reviewed :
Peer Reviewed verified by ORBi
Funders :
NSCF - National Natural Science Foundation of China [CN]
Available on ORBi :
since 17 January 2022

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