Oncotarget

Research Papers:

NOD2 up-regulates TLR2-mediated IL-23p19 expression via NF-κB subunit c-Rel in Paneth cell-like cells

Gao Tan, Erbo Liang, Kaili Liao, Feihong Deng, Wendi Zhang, Yuqing Chen, Jun Xu and Fachao Zhi _

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Oncotarget. 2016; 7:63651-63660. https://doi.org/10.18632/oncotarget.11467

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Abstract

Gao Tan1, Erbo Liang1,*, Kaili Liao1,*, Feihong Deng1,*, Wendi Zhang1,*, Yuqing Chen1,*, Jun Xu1,*, Fachao Zhi1

1Guangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China

*These authors have contributed equally to this work

Correspondence to:

Fachao Zhi, email: [email protected]

Keywords: interleukin-23p19, NOD2, Crohn's disease, intestinal immunity

Received: January 14, 2016    Accepted: August 13, 2016    Published: August 22, 2016

ABSTRACT

IL-23p19 plays important roles in intestinal antimicrobial immunity, while its over-expression can lead to intestinal inflammation. However, the bacterial compounds and the type of pattern recognition receptor involved in the inducible expression of IL-23p19 in Paneth cells remain unclear. Here we show that the mRNA expression of IL-23p19 was increased in Paneth cell (PC)-like cells stimulated by Toll-like receptor 2 (TLR2) ligands, peptidoglycan (PGN) and Pam3CSK4, and was further increased in the presence of nucleotide-binding oligomerization domain 2 (NOD2)-ligand muramyl dipeptide (MDP). However, its mRNA expression was decreased in NOD2-knockdown PC-like cells. Additionally, the c-Rel activation was increased in Pam3CSK4- or PGN-stimulated PC-like cells, but the PGN-induced c-Rel activation was decreased in NOD2-knockdown PC-like cells and had no significant difference compared with Pam3CSK4-induced c-Rel activation. Our results suggest that NOD2 up-regulates TLR2-mediated IL-23p19 expression via increasing c-Rel activation in PC-like cells. This finding might provide us with a novel therapeutic target for inflammatory bowel disease to inhibit IL-23p19 over-expression via the NOD2-c-Rel pathway.


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