A study on the mechanism of agonists in regulating transcriptional level of pIgR in salivary gland epithelial cells

激动剂调控涎腺上皮细胞pIgR转录水平的机制研究

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作者:Li Huang, Chuankong Sun, Ruobing Peng, Zhiming Liu

Abstract

The aim of the present study was to explore the mechanism of agonists in regulating transcriptional level of polymeric immunoglobulin receptor (pIgR) in salivary gland epithelial cells, thus revealing the defense effect of salivary immune on bacteria in the oral cavity. Sixty patients with oral bacterial infection and 70 patients suffering from oral diseases without bacterial infection were selected randomly from patients in Renmin Hospital of Wuhan University from April 2015 to April 2017. Ribonucleic acid (RNA) was extracted from salivary gland epithelial cells of all patients. Fluorescent quantitative polymerase chain reaction (FQ-PCR) and western blotting methods were adopted to detect and compare the transcriptional level of pIgR. The salivary gland epithelial cells of the 60 patients with oral bacterial infection were isolated and extracted, and they were divided into two groups (observation group and control group) randomly. Agonists were added to the observation group for acting for 24 h. FQ-PCR and immunofluorescence (IF) were adopted to detect and compare the transcriptional level of pIgR after acting with agonists. The toxicity of agonists on the cells was detected with Cell Counting kit-8 (CCK-8). The isolated salivary gland epithelial cells conformed to the morphology of epithelial cells, and adhered to the wall for growing. The transcriptional level of pIgR in the bacterial infection group was lower than that in the non-bacterial infection group (p<0.05). The transcriptional level of pIgR in the observation group was higher than that in the control group (p<0.05) after acting with agonists. Agonists can promote the rise of transcriptional level of pIgR in salivary gland epithelial cells, and the increase in pIgR is closely related to the cure of oral bacterial infection. Therefore, agonists can improve the oral immune function by regulating the transcription of pIgR.

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