Xie Rui-Di, Xu Ling-Zhi, Yang Li-Tao, Wang Shuai, Liu Qi, Liu Zhi-Gang, Yang Ping-Chang
The Research Center of Allergy & Immunology, Shenzhen University School of Medicine, Shenzhen, China.
Periodontal Department, the Affiliated Hospital of Zunyi Medical College, Zunyi, China.
Oncotarget. 2017 Feb 21;8(8):13214-13222. doi: 10.18632/oncotarget.14571.
The pathogenesis of oral-intestinal allergy syndrome (OIAS) has not been well understood. Published data indicate that galectin (Gal) 1 has immune regulatory functions. This study tests a hypothesis that Gal1 inhibits oral-intestinal allergy syndrome.
Mice were sensitized to peanut extracts (PE) via the buccal mucosa with or without using Gal1 together.
Upon re-exposure to specific antigen, the OIAS mice showed the systemic allergic response, the oral allergic reactions, and intestinal allergic inflammation, including increases in serum histamine, drop of the core temperature, higher levels of PE-specific IgE and interleukin (IL)-4. Increases in mast cell and eosinophil in the oral mucosa and intestinal mucosa were also observed. The OIAS was inhibited by co-administration with Gal1 via a mechanism of suppressing micro RNA (miR)-98 and reversing the expression of IL-10 in CD14+ cells in the intestine.
The OIAS can be induced by applying specific antigens to the oral mucosa, which can be inhibited by co-administration with Gal1.
口腔 - 肠道过敏综合征(OIAS)的发病机制尚未完全明确。已发表的数据表明半乳糖凝集素(Gal)1具有免疫调节功能。本研究旨在验证Gal1抑制口腔 - 肠道过敏综合征这一假说。
通过颊黏膜使小鼠对花生提取物(PE)致敏,同时使用或不使用Gal1。
再次接触特异性抗原后,OIAS小鼠出现全身过敏反应、口腔过敏反应和肠道过敏炎症,包括血清组胺增加、核心体温下降、PE特异性IgE和白细胞介素(IL)-4水平升高。在口腔黏膜和肠道黏膜中也观察到肥大细胞和嗜酸性粒细胞增多。通过抑制微小RNA(miR)-98并逆转肠道中CD14 +细胞中IL-10的表达机制,Gal1共同给药可抑制OIAS。
通过将特异性抗原应用于口腔黏膜可诱导OIAS,Gal1共同给药可抑制该综合征。