Wang Maowei, Yue Yan, Dong Chunsheng, Li Xiaoyun, Xu Wei, Xiong Sidong
Jiangsu Provincial Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Science, Soochow University, Suzhou, People's Republic of China.
Clin Vaccine Immunol. 2013 Nov;20(11):1743-51. doi: 10.1128/CVI.00466-13. Epub 2013 Sep 11.
Coxsackievirus B3 (CVB3), a small single-stranded RNA virus, belongs to the Picornaviridae family. Its infection is the most common cause of myocarditis, with no vaccine available. Gastrointestinal mucosa is the major entry port for CVB3; therefore, the induction of local immunity in mucosal tissues may help control initial viral infections and alleviate subsequent myocardial injury. Here we evaluated the ability of high-mobility group box 1 (HMGB1) encapsulated in chitosan particles to enhance the mucosal immune responses induced by the CVB3-specific mucosal DNA vaccine chitosan-pVP1. Mice were intranasally coimmunized with 4 doses of chitosan-pHMGB1 and chitosan-pVP1 plasmids, at 2-week intervals, and were challenged with CVB3 4 weeks after the last immunization. Compared with chitosan-pVP1 immunization alone, coimmunization with chitosan-pHMGB1 significantly (P < 0.05) enhanced CVB3-specific fecal secretory IgA levels and promoted mucosal T cell immune responses. In accordance, reduced severity of myocarditis was observed in coimmunized mice, as evidenced by significantly (P < 0.05) reduced viral loads, decreased myocardial injury, and increased survival rates. Flow cytometric analysis indicated that HMGB1 enhanced dendritic cell (DC) recruitment to mesenteric lymph nodes and promoted DC maturation, which might partly account for its mucosal adjuvant effect. This strategy may represent a promising approach to candidate vaccines against CVB3-induced myocarditis.
柯萨奇病毒B3(CVB3)是一种小型单链RNA病毒,属于微小核糖核酸病毒科。其感染是心肌炎最常见的病因,目前尚无可用疫苗。胃肠道黏膜是CVB3的主要侵入途径;因此,在黏膜组织中诱导局部免疫可能有助于控制初始病毒感染并减轻随后的心肌损伤。在此,我们评估了包裹在壳聚糖颗粒中的高迁移率族蛋白B1(HMGB1)增强CVB3特异性黏膜DNA疫苗壳聚糖-pVP1诱导的黏膜免疫反应的能力。小鼠每隔2周经鼻联合免疫4剂壳聚糖-pHMGB1和壳聚糖-pVP1质粒,并在最后一次免疫后4周用CVB3攻击。与单独免疫壳聚糖-pVP1相比,联合免疫壳聚糖-pHMGB1显著(P < 0.05)提高了CVB3特异性粪便分泌型IgA水平,并促进了黏膜T细胞免疫反应。相应地,联合免疫的小鼠心肌炎严重程度降低,表现为病毒载量显著(P < 0.05)降低、心肌损伤减轻和存活率提高。流式细胞术分析表明,HMGB1增强了树突状细胞(DC)向肠系膜淋巴结的募集并促进了DC成熟,这可能部分解释了其黏膜佐剂作用。该策略可能是一种有前景的抗CVB3诱导心肌炎候选疫苗方法。