Abstract
Background and aims Neutrophilic inflammation is a hallmark of some specific asthma phenotypes; its aetiology is not yet fully understood. House dust mite (HDM) is the most common factor in the pathogenesis of airway inflammation. This study aims to elucidate the role of cross-antibodies against HDM-derived factors in the development of neutrophilic inflammation in the airway.
Methods Blood samples were collected from asthma patients with chronic neutrophilic asthma for analysis of HDM-specific cross-reactive antibodies. The role of an antibody against HDM-derived enolase (EnoAb) in the impairment of airway epithelial barrier function and induction of airway inflammation was assessed in a cell culture model and an animal model.
Results High similarity (72%) of the enolase gene sequences was identified between HDM and human. Serum EnoAb was detected in patients with chronic neutrophilic asthma. The EnoAb bound to airway epithelial cells to form complexes with enolase, which activated complement, impaired airway epithelial barrier functions and induced neutrophilic inflammation in the airway tissues.
Conclusions HDM-derived enolase can induce specific cross-antibodies in humans, which induce neutrophilic inflammation in the airway.
Abstract
House dust mite (HDM)-derived enolase induces cross-antibodies in the body, which recognise both HDM-derived enolase and the enolase in the airway epithelial cells, activate complement and induce neutrophilic inflammation in the airway tissues https://bit.ly/2XKSCgy
Footnotes
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Author contributions: J. Lin, N. Huang, J. Li, X. Liu, Q. Xiong, C. Hu, D. Chen, L. Guan, K. Chang and D. Li performed experiments and analysed data. S.K-W. Tsui provided bioinformatic analysis. J. Li provided clinical materials. P-C. Yang, Z. Liu and N. Zhong organised the study and supervised experiments. P-C. Yang, Z. Liu and J. Lin designed the project. P-C. Yang wrote the manuscript. All authors reviewed the manuscript.
Conflict of interest: J. Lin has nothing to disclose.
Conflict of interest: N. Huang has nothing to disclose.
Conflict of interest: J. Li has nothing to disclose.
Conflict of interest: X. Liu has nothing to disclose.
Conflict of interest: Q. Xiong has nothing to disclose.
Conflict of interest: C. Hu has nothing to disclose.
Conflict of interest: D. Chen has nothing to disclose.
Conflict of interest: L. Guan has nothing to disclose.
Conflict of interest: K. Chang has nothing to disclose.
Conflict of interest: D. Li has nothing to disclose.
Conflict of interest: S.K-W. Tsui has nothing to disclose.
Conflict of interest: N. Zhong has nothing to disclose.
Conflict of interest: Z. Liu has nothing to disclose.
Conflict of interest: P-C. Yang has nothing to disclose.
Support statement: This study was supported by grants from the National Key Research and Development Program on Precision Medicine (No.2016YFC0905802, 2016YFC0903700), Natural Science Foundation of China (31729002, 91542104, 31570932), Science and technology project of Guangdong Province (No.2014B090901041, 2016A020216029), Opening fund of State Key Laboratory of Respiratory Disease (No.SKLRD2016ZJ001), Shenzhen Scientific Technology Basic Research Projects (No.KQTD20170331145453160, JCYJ20160328144536436, KQJSCX20180328095619081), Shenzhen Nanshan District Pioneer Group Research Funds (No.LHTD20180007) and Guangdong Provincial Key Laboratory of Regional Immunity and Diseases (2019B030301009).
- Received December 11, 2019.
- Accepted July 30, 2020.
- Copyright ©ERS 2021
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