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气道上皮细胞 ITGB4 缺乏加重 RSV 感染并增加对 HDM 的敏感性。

ITGB4 Deficiency in Airway Epithelium Aggravates RSV Infection and Increases HDM Sensitivity.

机构信息

Department of Respiratory Medicine, National Clinical Research Center for Respiratory Diseases, Xiangya Hospital, Central South University, Changsha, China.

Department of Physiology, School of Basic Medicine Science, Central South University, Changsha, China.

出版信息

Front Immunol. 2022 Jul 25;13:912095. doi: 10.3389/fimmu.2022.912095. eCollection 2022.

DOI:10.3389/fimmu.2022.912095
PMID:35958591
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9357881/
Abstract

BACKGROUND

The heterogeneity of RSV-infected pathology phenotype in early life is strongly associate with increased susceptibility of asthma in later life. However, the inner mechanism of this heterogeneity is still obscure. ITGB4 is a down-regulated adhesion molecular in the airway epithelia of asthma patients which may participate in the regulation of RSV infection related intracellular pathways.

OBJECT

This study was designed to observe the involvement of ITGB4 in the process of RSV infection and the effect of ITGB4 deficiency on anti-RSV responses of airway epithelia.

RESULTS

RSV infection caused a transient decrease of ITGB4 expression both and . Besides, ITGB4 deficiency induced not only exacerbated RSV infection, but also enhanced HDM sensitivity in later life. Moreover, IFN III (IFN-λ) was significantly suppressed during RSV infection in ITGB4 deficient airway epithelial cells. Furthermore, the suppression of IFN-λ were regulated by IRF-1 through the phosphorylation of EGFR in airway epithelial cells after RSV infection.

CONCLUSION

These results demonstrated the involvement of ITGB4 deficiency in the development of enhance RSV infection in early life and the increased HDM sensitivity in later life by down-regulation of IFN-λ through EGFR/IRF-1 pathway in airway epithelial cells.

摘要

背景

在生命早期，呼吸道合胞病毒（RSV）感染的病理学表型的异质性与生命后期哮喘易感性的增加密切相关。然而，这种异质性的内在机制尚不清楚。ITGB4 是哮喘患者气道上皮细胞中下调的黏附分子，可能参与 RSV 感染相关的细胞内途径的调节。

目的

本研究旨在观察 ITGB4 在 RSV 感染过程中的作用，以及 ITGB4 缺失对气道上皮细胞抗 RSV 反应的影响。

结果

RSV 感染导致 ITGB4 表达在 和 时短暂下降。此外，ITGB4 缺失不仅导致 RSV 感染加重，而且导致生命后期对 HDM 的敏感性增强。此外，在 ITGB4 缺陷的气道上皮细胞中，IFN-λ 在 RSV 感染期间显著受到抑制。此外，在 RSV 感染后，EGFR/IRF-1 通路通过气道上皮细胞中 EGFR 的磷酸化调节 IFN-λ 的抑制。

结论

这些结果表明，ITGB4 缺失通过 EGFR/IRF-1 通路下调 IFN-λ，参与了生命早期增强 RSV 感染的发展，以及生命后期对 HDM 敏感性的增加。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4943/9357881/ed7819913e42/fimmu-13-912095-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4943/9357881/ccd585624a5f/fimmu-13-912095-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4943/9357881/a5c13c255852/fimmu-13-912095-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4943/9357881/1dc34a6cf049/fimmu-13-912095-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4943/9357881/5dffad5f058b/fimmu-13-912095-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4943/9357881/0b86db9a0f1d/fimmu-13-912095-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4943/9357881/65144f4cc75f/fimmu-13-912095-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4943/9357881/ed7819913e42/fimmu-13-912095-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4943/9357881/ccd585624a5f/fimmu-13-912095-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4943/9357881/a5c13c255852/fimmu-13-912095-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4943/9357881/1dc34a6cf049/fimmu-13-912095-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4943/9357881/5dffad5f058b/fimmu-13-912095-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4943/9357881/0b86db9a0f1d/fimmu-13-912095-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4943/9357881/65144f4cc75f/fimmu-13-912095-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4943/9357881/ed7819913e42/fimmu-13-912095-g007.jpg

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