Endoplasmic reticulum stress is upregulated in inflammatory bowel disease and contributed TLR2 pathway-mediated inflammatory response

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成果类型：

期刊论文

作者：

Wu, Weijie;Zhao, Yan;Hu, Tian;Long, Yan;Zeng, Ya;...

通讯作者：

Shen, YM

作者机构：

[Wu, Weijie; Shen, Yueming; Li, Mengling; Peng, Siyuan; Zeng, Ya; Long, Yan; Hu, Tian] Univ South China, Dept Digest Dis, Changsha Cent Hosp, Changsha, Hunan, Peoples R China.

[Zhao, Yan] Univ South China, Dept Pathol, Changsha Cent Hosp, Changsha, Hunan, Peoples R China.

[Hu, Jinyue] Univ South China, Cent Lab, Changsha Cent Hosp, Changsha, Hunan, Peoples R China.

[Shen, Yueming; Shen, YM] Univ South china, Dept Digest Dis, Changsha Cent Hosp, 161 Shaoshan nanlu, Changsha, Hunan, Peoples R China.

通讯机构：

[Shen, YM ] U

Univ South china, Dept Digest Dis, Changsha Cent Hosp, 161 Shaoshan nanlu, Changsha, Hunan, Peoples R China.

语种：

英文

关键词：

inflammatory bowel disease;endoplasmic reticulum stress;TLR2;GRP78;TNF-a

期刊：

Immunopharmacology and Immunotoxicology

ISSN：

0892-3973

年：

2023

卷：

期：

页码：

DOI：

10.1080/08923973.2023.2298897

基金类别：

This study was supported by grants from Hunan Science and Technology Innovation Plan Project (No. 2020SK53306) and Natural Science Foundation of Hunan Province (No. 2023JJ30067). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

机构署名：

本校为第一且通讯机构

院系归属：

医学院

摘要：

OBJECTIVE: Endoplasmic reticulum stress (ERS) and Toll-like receptor 2 (TLR2) signaling play an important role in inflammatory bowel disease (IBD); however, the link between TLR2 and ERS in IBD is unclear. This study investigated whether Thapsigargin (TG) -induced ER protein expression levels contributed to TLR2-mediated inflammatory response. METHODS: The THP-1 cells were treated with TLR2 agonist (Pam3CSK4), ERS inducer Thapsigargin (TG) or inhibitor (TUDCA). The mRNA expressions of TLR1-TLR10 were detected by qPCR. The production and secreti...

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Endoplasmic reticulum stress is upregulated in inflammatory bowel disease and contributed TLR2 pathway-mediated inflammatory response

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