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Repeated exposure to inactivated Streptococcus pneumoniae induces asthma-like pathological changes in mice in the presence of IL-33

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Chenduo Li, Xiaonan Du, Qiong Huang, Yiran Yang, Jingjing Wang, Xiaofeng Qin, Wenjun Wang, Zihan Liu, Huihui Yuan, Jie Liu, Zhe Lv, Yan Li, Yan Chen, Ye Cui, Chris J. Corrigan, Kewu Huang, Wei Wang, Sun Ying

Original languageEnglish
Article number104438
JournalCellular Immunology
Volume369
DOIs
PublishedNov 2021

Bibliographical note

Funding Information: We are grateful for financial support from the National Natural Science Foundation of China [82071805, 81700026, 81971510], Beijing Natural Science Foundation [7192023], and the Support Project of High-level Teachers in Beijing Municipal Universities in the Period of 13th Five–year Plan (IDHT20190510). Funding Information: We are grateful for financial support from the National Natural Science Foundation of China [82071805, 81700026, 81971510], Beijing Natural Science Foundation [7192023], and the Support Project of High-level Teachers in Beijing Municipal Universities in the Period of 13th Five?year Plan (IDHT20190510). Publisher Copyright: © 2021 Elsevier Inc. Copyright: Copyright 2021 Elsevier B.V., All rights reserved.

King's Authors

Abstract

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.

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