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PDIA3 gene induces visceral hypersensitivity in rats with irritable bowel syndrome through the dendritic cell-mediated activation of T cells
Author(s) -
Zhaomeng Zhuang,
Lu Zhang,
Xiaoteng Wang,
Liyuan Tao,
Bin Lv
Publication year - 2016
Publication title -
peerj
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.927
H-Index - 70
ISSN - 2167-8359
DOI - 10.7717/peerj.2644
Subject(s) - irritable bowel syndrome , degranulation , gene knockdown , cd8 , mesenteric lymph nodes , t cell , protein disulfide isomerase , immunology , cytotoxic t cell , chemistry , medicine , microbiology and biotechnology , endocrinology , immune system , biology , receptor , gene , biochemistry , endoplasmic reticulum , in vitro
This study investigated the mechanism of protein disulfide-isomerase A3 (PDIA3)-induced visceral hypersensitivity in irritable bowel syndrome (IBS). Rats were treated with saline (control), acetic acid and restraint stress (IBS model), empty vector (RNAi control) and PDIA3-RNAi vector (PDIA3-RNAi). Mesenteric lymph node DCs (MLNDCs) and splenic CD4+/CD8+ T cells were isolated for co-cultivation. Compared with control, MLNDCs co-cultured with CD4+ or CD8+ T cells showed an increased ability to promote T cell proliferation and produced more IL-4 or IL-9 secretion. Compared with the RNAi control, MLNDCs from the PDIA3 knockdown models were less effective in promoting the proliferation of CD4+/CD8+ T cells. It is concluded that PDIA3 plays an important role in the development of IBS through the DC-mediated activation of T cells, resulting in degranulation of MCs and visceral hypersensitivity.

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