论文部分内容阅读
目的研究维生素A缺乏(vitamin A deficiency,VAD)对大鼠肠粘膜树突状细胞(dendritic cell,DC)数量、成熟度和抗原识别的影响,及其在肠道感染时的变化,探讨VAD调节肠粘膜抗感染免疫的机制。方法在建立VAD大鼠模型的基础上,给予鼠伤寒沙门氏菌灌胃诱导肠道感染。取新鲜回肠组织,采用免疫组化和RT-PCR法,观察肠粘膜DC数目(OX一62阳性细胞数)、成熟度(CD80、CCR7的阳性面积);抗原识别受体表达水平(TLR2和TLR4的阳性面积)和信号转导(MyD88的基因转录水平)。结果 VAD与VA正常大鼠比较,肠粘膜DC的数目显著增加,当合并感染时不仅DC数量而且成熟分化标志CCR7也明显增加。肠集合淋巴小结中TLR2、TLR4的蛋白表达都明显升高,在合并感染后TLR2的表达上调更明显,MyD88 mRNA水平上调。结论 VAD大鼠粘膜DC的增多和活化可能是诱导炎症反应增强,导致粘膜损伤的重要机制之一。
Objective To investigate the effect of vitamin A deficiency (VAD) on the number, maturity and antigenicity of dendritic cells (DCs) in intestinal mucosa of rats and their changes during intestinal infection, Intestinal mucosal anti-infection immune mechanism. Methods Based on the establishment of VAD rat model, Salmonella typhimurium was given intragastrically to induce intestinal infection. Immunohistochemistry and RT-PCR were used to observe the number of intestinal mucosa (OX-62 positive cells), maturation (positive area of CD80 and CCR7), antigen receptor expression (TLR2 and TLR4 Positive area) and signal transduction (MyD88 gene transcription level). Results Compared with normal rats, VAD significantly increased the number of intestinal mucosal DCs. When co-infected, not only the number of DC but also the mature differentiation marker CCR7 was significantly increased. The expression of TLR2 and TLR4 protein in intestinal aggregated lymphoid tissues were significantly increased. The expression of TLR2 was significantly up-regulated and MyD88 mRNA was up-regulated after co-infection. Conclusions The increase and activation of mucosal DC in VAD rats may be one of the important mechanisms that induce the enhancement of inflammatory reaction and cause mucosal injury.