1. Repeated exposure to inactivated Streptococcus pneumoniae induces asthma-like pathological changes in mice in the presence of IL-33.
- Author
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Li, Chenduo, Du, Xiaonan, Huang, Qiong, Yang, Yiran, Wang, Jingjing, Qin, Xiaofeng, Wang, Wenjun, Liu, Zihan, Yuan, Huihui, Liu, Jie, Lv, Zhe, Li, Yan, Chen, Yan, Cui, Ye, Corrigan, Chris J., Huang, Kewu, Wang, Wei, and Ying, Sun
- Subjects
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PATHOLOGICAL physiology , *INTERLEUKIN-33 , *STREPTOCOCCUS pneumoniae , *BACTERIAL antigens , *ASTHMATICS - Abstract
• Repeated exposure of IL-33 with S. pneumoniae induced asthma-like changes. • S. pneumoniae was able to increase airways hyperresponsiveness and inflammation. • S. pneumoniae lysates-specific IgE was significantly elevated in the asthma patients. • These suggest that bacterial antigens might be potential allergens for atopic asthma. While environmental aeroallergens and epithelial alarmins such as IL-33 are firmly implicated in asthma, the possible role of Streptococcus pneumoniae (S. pneumoniae) antigens is less clear. To explore this, wild-type BALB/c mice were repeatedly challenged per-nasally with IL-33 and inactivated S. pneumoniae , either agent alone or diluent control. Some animals were rested then later re-challenged with inactivated S. pneumoniae alone. Serum concentrations of S. pneumoniae lysates-specific IgE were measured in patients with asthma and control subjects. Interestingly, in the presence of IL-33, repeated exposure to inactivated S. pneumoniae induced asthma-like pathological changes accompanied by a systemic adaptive immune response. Subsequent re-exposure of the sensitized animals to inactivated S. pneumoniae alone was able to induce such changes. The concentration of S. pneumoniae lysates-specific IgE was significantly elevated in the asthma patients. These data suggest that antigens derived from infectious microorganisms may participate in generating the mucosal inflammation which characterizes asthma. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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