Abstract
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 CD4C/CD8C T cells were isolated for co-cultivation. Compared with control, MLNDCs co-cultured with CD4C or CD8C 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 CD4C/CD8C 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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Zhuang, Z., Zhang, L., Wang, X., Tao, L., & Lv, B. (2016). PDIA3 gene induces visceral hypersensitivity in rats with irritable bowel syndrome through the dendritic cell-mediated activation of T cells. PeerJ, 2016(11). https://doi.org/10.7717/peerj.2644
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