中文摘要：本研究发现，肺炎支原体产生的ADP-核糖化和空泡毒素即社区获得性呼吸窘迫综合征毒素（CARDS 毒素）能够有效加重小鼠变态反应性炎症和哮喘类疾病。研究利用CARDS 毒素暴露小鼠模型评价了总血浆IgE反应和CARDS毒素特异性血浆IgE反应。研究发现，单一的粘膜CARDS毒素暴露足以提高小鼠血浆总IgE和CARDS毒素特异性IgE水平。小鼠二次粘膜暴露CARDS毒素显著提高了总IgE和CARDS毒素特异性IgE水平。CARDS毒素特异性IgE与CARDS毒素N-末端肽相关，但与C-末端肽不相关。同时，全长CARDS毒素和N-末端肽会导致肥大细胞脱粒。总而言之，CARDS毒素暴露足以让小鼠产生功能性IgE，肺炎支原体和CARDS毒素与哮喘加重密切相关，CARDS毒素-特异性IgE-肥大细胞轴可能与疾病发生相关。
外文摘要：Mycoplasma pneumoniae is strongly associated with new onset asthma and asthma exacerbations. Until recently, the molecular mechanisms utilized by M. pneumoniae to influence asthma symptoms were unknown. However, we recently reported that an ADP-ribosylating and vacuolating toxin called the Community Acquired Respiratory Distress Syndrome toxin, CARDS toxin, produced by M. pneumoniae was sufficient to promote allergic inflammation and asthma-like disease in mice. A mouse model of CARDS toxin exposure was used to evaluate total and CARDS-toxin specific serum IgE responses. Mast cell sensitization, challenge, and degranulation studies determined functionality of the CARDS toxin-specific IgE. In the current study, we report that a single mucosal exposure to CARDS toxin was sufficient to increase total serum IgE and CARDS toxin-specific IgE in mice. Mice given a second mucosal challenge of CARDS toxin responded with significant increases in total and CARDS toxin-specific IgE. CARDS toxin-specific IgE bound to an N-terminal peptide of CARDS toxin but not the C-terminal peptide. Likewise, full-length CARDS toxin and the N-terminal peptide induced mast cell degranulation. Altogether, these data demonstrate that exposure to CARDS toxin is sufficient to generate functional IgE in mice. M. pneumoniae and CARDS toxin are strongly associated with asthma exacerbations raising the possibility that the CARDS toxin-specific IgE-mast cell axis contributes to disease pathogenesis.
外文关键词：MAST-CELLS PROTECT; IMMUNOGLOBULIN-E; PULMONARY INFLAMMATION; VACUOLATING CYTOTOXIN; PERTUSSIS TOXIN; CHRONIC ASTHMA; INFECTION; CHILDREN; ALLERGY; RISK
作者：Medina, JL; Brooks, EG; Chaparro, A; Dube, PH
作者单位：德克萨斯大学保健科学中心
期刊名称：PLOS ONE
期刊影响因子：3.057
出版年份：2017
出版刊次：2
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