Matsumoto Hisako, Kanemitsu Yoshihiro, Nagasaki Tadao, Tohda Yuji, Horiguchi Takahiko, Kita Hideo, Kuwabara Kazunobu, Tomii Keisuke, Otsuka Kojiro, Fujimura Masaki, Ohkura Noriyuki, Tomita Katsuyuki, Yokoyama Akihito, Ohnishi Hiroshi, Nakano Yasutaka, Oguma Tetsuya, Hozawa Soichiro, Izuhara Yumi, Ito Isao, Oguma Tsuyoshi, Inoue Hideki, Tajiri Tomoko, Iwata Toshiyuki, Ono Junya, Ohta Shoichiro, Hirota Tomomitsu, Kawaguchi Takahisa, Tamari Mayumi, Yokoyama Tetsuji, Tabara Yasuharu, Matsuda Fumihiko, Izuhara Kenji, Niimi Akio, Mishima Michiaki
Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Kinki Hokuriku Airway Disease Conference, Osaka, Japan.
Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Kinki Hokuriku Airway Disease Conference, Osaka, Japan.
Ann Allergy Asthma Immunol. 2017 Feb;118(2):197-203. doi: 10.1016/j.anai.2016.11.013. Epub 2016 Dec 27.
Sensitization to Staphylococcus aureus enterotoxin (SE) is a known risk factor for asthma susceptibility and severity. However, how SE sensitization is involved in asthma, particularly nonatopic asthma and/or late-onset asthma, remains uncertain.
To clarify the involvement of SE sensitization in nonatopic and/or late-onset asthma and its association with a polymorphism of the cysteinyl leukotriene receptor 1 gene (CysLTR1), which was examined because CysLT signaling is closely associated with late-onset eosinophilic asthma.
We assessed associations between sensitization to SE (A and/or B) and clinical indexes in 224 patients with asthma (mean age, 62.3 years; 171 women) from a cohort of the Kinki Hokuriku Airway Disease Conference, particularly those with nonatopic asthma (not sensitized to common aeroallergens) and/or late-onset asthma. Associations between SE sensitization and CysLTR1 polymorphism (rs2806489), a potential regulatory variant for atopic predisposition in women, were also assessed in a sex-stratified manner.
A total of 105 patients (47%) with asthma were sensitized to SE. Among patients with nonatopic asthma (n = 67) or with late-onset asthma (n = 124), those sensitized to SE had significantly higher serum total IgE and periostin levels than those not sensitized. In nonatopic patients, a rapid decrease in forced expiratory volume in 1 second was associated with SE sensitization. In women with asthma, rs2806489 was associated with sensitization to SEB and age at asthma onset.
SE sensitization contributes to T2 inflammation in nonatopic and/or late-onset asthma. In women with asthma, the CysLTR1 variant might be associated with sensitization to SEB and age at asthma onset.
对金黄色葡萄球菌肠毒素（SE）致敏是哮喘易感性和严重程度的已知危险因素。然而，SE致敏如何参与哮喘，尤其是非特应性哮喘和/或迟发性哮喘，仍不确定。
阐明SE致敏在非特应性和/或迟发性哮喘中的作用及其与半胱氨酰白三烯受体1基因（CysLTR1）多态性的关联，由于CysLT信号通路与迟发性嗜酸性粒细胞性哮喘密切相关，因此对其进行了检测。
我们评估了来自近畿北陆气道疾病会议队列的224例哮喘患者（平均年龄62.3岁；171名女性）中SE（A和/或B）致敏与临床指标之间的关联，特别是那些患有非特应性哮喘（对常见气传变应原未致敏）和/或迟发性哮喘的患者。还按性别分层评估了SE致敏与CysLTR1多态性（rs2806489）之间的关联，CysLTR1多态性是女性特应性易感性的潜在调节变体。
共有105例（47%）哮喘患者对SE致敏。在非特应性哮喘患者（n = 67）或迟发性哮喘患者（n = 124）中，对SE致敏的患者血清总IgE和骨膜蛋白水平显著高于未致敏患者。在非特应性患者中，1秒用力呼气量的快速下降与SE致敏有关。在哮喘女性患者中，rs2806489与对SEB的致敏和哮喘发病年龄有关。
SE致敏在非特应性和/或迟发性哮喘中促成2型炎症。在哮喘女性患者中，CysLTR1变体可能与对SEB的致敏和哮喘发病年龄有关。
