摘要
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 influence of vitamin A deficiency（VAD） on the immnnolagical response of intestinal mucosal dendritic cells（DC） in rats to intestinal infection and its mechanism.Method The rat model with VAD was established,and intestinal infection was induced by giving typhoid Salmonella orally.The fresh ileum tissue samples were taken and the effect of VA on the number and maturation of DC,as well as antigen recognition receptors in mucosa was detected by immunohistochemical and RT PCR methods.Results Compared with normal rats,the numbers of DC in intestinal mucosa of VAD rats were increased and both the number and maturation of DC were promoted.When VAD was complicated with infection,The expressions of TLR2 and TLR4 were elevated in mucosa,and higher expression of TLR2 was found in infected intestinal mucosa of VAD rats.Conclusion The increase of the number and activation of mucosal DC may play important roles in inflammatory reactions and impairment of mucosa in VAD rats.
出处
《营养学报》
CAS
CSCD
北大核心
2011年第4期358-361,366,共5页
Acta Nutrimenta Sinica
基金
国家自然科学基金(No.30371210)
