Imperial College London
Alternate

DrYoumingZhang

Faculty of Medicine, National Heart & Lung Institute

Lecturer (non-clinical) in Respiratory Genomics
 
 
 
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Contact

 

+44 (0)20 7594 7974y.zhang

 
 
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Location

 

413Guy Scadding BuildingRoyal Brompton Campus

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Summary

 

Publications

Citation

BibTex format

@article{Li:2023:10.1186/s12931-023-02406-5,
author = {Li, J and Zheng, Z and Liu, Y and Zhang, H and Zhang, Y and Gao, G},
doi = {10.1186/s12931-023-02406-5},
journal = {Respiratory Research},
pages = {1--12},
title = {IRAK-M has effects in regulation of lung epithelial inflammation},
url = {http://dx.doi.org/10.1186/s12931-023-02406-5},
volume = {24},
year = {2023}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - BackgroundEpithelial barrier is important for asthma development by shaping immune responses. Airway expressing-IL-1 receptor-associated kinase (IRAK)-M of Toll-like receptor pathway was involved in immunoregulation of airway inflammation through influencing activities of macrophages and dendritic cells or T cell differentiation. Whether IRAK-M has effect on cellular immunity in airway epithelial cells upon stimulation remains unclear.MethodsWe modeled cellular inflammation induced by IL-1β, TNF-α, IL-33, and house dust mite (HDM) in BEAS-2B and A549 cells. Cytokine production and pathway activation were used to reflect the effects of IRAK-M siRNA knockdown on epithelial immunity. Genotyping an asthma-susceptible IRAK-M SNP rs1624395 and measurement of serum CXCL10 levels were performed in asthma patients.ResultsIRAK-M expression was significantly induced in BEAS-2B and A549 cells after inflammatory stimulation. IRAK-M knockdown increased the lung epithelial production of cytokines and chemokines, including IL-6, IL-8, CXCL10, and CXCL11, at both mRNA and protein levels. Upon stimulation, IRAK-M silencing led to overactivation of JNK and p38 MAPK in lung epithelial cells. While antagonizing JNK or p38 MAPK inhibited increased secretion of CXCL10 in IRAK-M silenced-lung epithelium. Asthma patients carrying G/G genotypes had significantly higher levels of serum CXCL10 than those carrying homozygote A/A.ConclusionOur findings suggested that IRAK-M has effect on lung epithelial inflammation with an influence on epithelial secretion of CXCL10 partly mediated through JNK and p38 MAPK pathways. IRAK-M modulation might indicate a new insight into asthma pathogenesis from disease origin.
AU  - Li,J
AU  - Zheng,Z
AU  - Liu,Y
AU  - Zhang,H
AU  - Zhang,Y
AU  - Gao,G
DO  - 10.1186/s12931-023-02406-5
EP  - 12
PY  - 2023///
SN  - 1465-9921
SP  - 1
TI  - IRAK-M has effects in regulation of lung epithelial inflammation
T2  - Respiratory Research
UR  - http://dx.doi.org/10.1186/s12931-023-02406-5
UR  - https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-023-02406-5
UR  - http://hdl.handle.net/10044/1/103598
VL  - 24
ER  -
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