Stress granule assembly impairs macrophage efferocytosis to aggravate allergic rhinitis in mice

Abstract Cytoplasmic stress granules (SG) assemble in response to stress-induced translational arrest and are key signaling hubs orchestrating cell fate and regulating various physiological and pathological processes. However, the role of SG formation in the progression of allergic diseases is incom...

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Main Authors: Ye Zhou, Zixuan Yang, Yuanyuan Wang, Yue Dong, Tianyu Wang, Yunhui Li, Caiquan Liang, Yanfang Liu, Zhixuan Li, Shanrong Liu, Liangchen Gui, Yiwen Fan, Ting Lei, Kaiwei Jia, Liyuan Zhang, Mu Wang, Wen Nie, Long Chen, Mingrui Ma, Yanfeng Wu, Cuiping Zhong, Huanhai Liu, Jin Hou
Format: Article
Language:English
Published: Nature Portfolio 2025-07-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-60920-0
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author Ye Zhou
Zixuan Yang
Yuanyuan Wang
Yue Dong
Tianyu Wang
Yunhui Li
Caiquan Liang
Yanfang Liu
Zhixuan Li
Shanrong Liu
Liangchen Gui
Yiwen Fan
Ting Lei
Kaiwei Jia
Liyuan Zhang
Mu Wang
Wen Nie
Long Chen
Mingrui Ma
Yanfeng Wu
Cuiping Zhong
Huanhai Liu
Jin Hou
author_facet Ye Zhou
Zixuan Yang
Yuanyuan Wang
Yue Dong
Tianyu Wang
Yunhui Li
Caiquan Liang
Yanfang Liu
Zhixuan Li
Shanrong Liu
Liangchen Gui
Yiwen Fan
Ting Lei
Kaiwei Jia
Liyuan Zhang
Mu Wang
Wen Nie
Long Chen
Mingrui Ma
Yanfeng Wu
Cuiping Zhong
Huanhai Liu
Jin Hou
author_sort Ye Zhou
collection DOAJ
description Abstract Cytoplasmic stress granules (SG) assemble in response to stress-induced translational arrest and are key signaling hubs orchestrating cell fate and regulating various physiological and pathological processes. However, the role of SG formation in the progression of allergic diseases is incompletely understood. Here, by analyzing the nasal tissues of allergic rhinitis (AR) mouse models and AR patients, we find that SGs assemble specifically in the macrophages within the nasal mucosa and promote AR progression by restraining the efferocytotic ability of macrophages, ultimately resulting in reduced Mres generation and IL-10 production. Mechanistically, intracellular m7G-modified Lrp1 mRNA, encoding for a typical efferocytosis receptor, is transported by the m7G reader QKI7 into stress-induced SGs, where Lrp1 mRNA is sequestered away from the translation machinery, ultimately resulting in reduced macrophage efferocytosis. Therefore, SG assembly impairs macrophage efferocytosis and aggravates AR, and the inhibition of SGs bears considerable potential in the targeted therapy.
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issn 2041-1723
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publisher Nature Portfolio
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series Nature Communications
spelling doaj-art-0c88d94d4d70466e985dc2045b34fc142025-08-20T03:03:44ZengNature PortfolioNature Communications2041-17232025-07-0116111810.1038/s41467-025-60920-0Stress granule assembly impairs macrophage efferocytosis to aggravate allergic rhinitis in miceYe Zhou0Zixuan Yang1Yuanyuan Wang2Yue Dong3Tianyu Wang4Yunhui Li5Caiquan Liang6Yanfang Liu7Zhixuan Li8Shanrong Liu9Liangchen Gui10Yiwen Fan11Ting Lei12Kaiwei Jia13Liyuan Zhang14Mu Wang15Wen Nie16Long Chen17Mingrui Ma18Yanfeng Wu19Cuiping Zhong20Huanhai Liu21Jin Hou22National Key Laboratory of Immunity and Inflammation, Second Military Medical UniversityDepartment of Otolaryngology-Head and Neck Surgery, Second Affiliated Hospital of Second Military Medical UniversityNational Key Laboratory of Immunity and Inflammation, Second Military Medical UniversityNational Key Laboratory of Immunity and Inflammation, Second Military Medical UniversityDepartment of Otolaryngology-Head and Neck Surgery, Second Affiliated Hospital of Second Military Medical UniversityNational Key Laboratory of Immunity and Inflammation, Second Military Medical UniversityDepartment of Otolaryngology-Head and Neck Surgery, Second Affiliated Hospital of Second Military Medical UniversityNational Key Laboratory of Immunity and Inflammation, Second Military Medical UniversityNational Key Laboratory of Immunity and Inflammation, Second Military Medical UniversityNational Key Laboratory of Immunity and Inflammation, Second Military Medical UniversityNational Key Laboratory of Immunity and Inflammation, Second Military Medical UniversityNational Key Laboratory of Immunity and Inflammation, Second Military Medical UniversityNational Key Laboratory of Immunity and Inflammation, Second Military Medical UniversityNational Key Laboratory of Immunity and Inflammation, Second Military Medical UniversityNational Key Laboratory of Immunity and Inflammation, Second Military Medical UniversityNational Key Laboratory of Immunity and Inflammation, Second Military Medical UniversityNational Key Laboratory of Immunity and Inflammation, Second Military Medical UniversityNational Key Laboratory of Immunity and Inflammation, Second Military Medical UniversityNational Key Laboratory of Immunity and Inflammation, Second Military Medical UniversityNational Key Laboratory of Immunity and Inflammation, Second Military Medical UniversityDepartment of Otolaryngology-Head and Neck Surgery, No. 940 Hospital of Joint Logistics Support Force of People’s Liberation ArmyDepartment of Otolaryngology-Head and Neck Surgery, Second Affiliated Hospital of Second Military Medical UniversityNational Key Laboratory of Immunity and Inflammation, Second Military Medical UniversityAbstract Cytoplasmic stress granules (SG) assemble in response to stress-induced translational arrest and are key signaling hubs orchestrating cell fate and regulating various physiological and pathological processes. However, the role of SG formation in the progression of allergic diseases is incompletely understood. Here, by analyzing the nasal tissues of allergic rhinitis (AR) mouse models and AR patients, we find that SGs assemble specifically in the macrophages within the nasal mucosa and promote AR progression by restraining the efferocytotic ability of macrophages, ultimately resulting in reduced Mres generation and IL-10 production. Mechanistically, intracellular m7G-modified Lrp1 mRNA, encoding for a typical efferocytosis receptor, is transported by the m7G reader QKI7 into stress-induced SGs, where Lrp1 mRNA is sequestered away from the translation machinery, ultimately resulting in reduced macrophage efferocytosis. Therefore, SG assembly impairs macrophage efferocytosis and aggravates AR, and the inhibition of SGs bears considerable potential in the targeted therapy.https://doi.org/10.1038/s41467-025-60920-0
spellingShingle Ye Zhou
Zixuan Yang
Yuanyuan Wang
Yue Dong
Tianyu Wang
Yunhui Li
Caiquan Liang
Yanfang Liu
Zhixuan Li
Shanrong Liu
Liangchen Gui
Yiwen Fan
Ting Lei
Kaiwei Jia
Liyuan Zhang
Mu Wang
Wen Nie
Long Chen
Mingrui Ma
Yanfeng Wu
Cuiping Zhong
Huanhai Liu
Jin Hou
Stress granule assembly impairs macrophage efferocytosis to aggravate allergic rhinitis in mice
Nature Communications
title Stress granule assembly impairs macrophage efferocytosis to aggravate allergic rhinitis in mice
title_full Stress granule assembly impairs macrophage efferocytosis to aggravate allergic rhinitis in mice
title_fullStr Stress granule assembly impairs macrophage efferocytosis to aggravate allergic rhinitis in mice
title_full_unstemmed Stress granule assembly impairs macrophage efferocytosis to aggravate allergic rhinitis in mice
title_short Stress granule assembly impairs macrophage efferocytosis to aggravate allergic rhinitis in mice
title_sort stress granule assembly impairs macrophage efferocytosis to aggravate allergic rhinitis in mice
url https://doi.org/10.1038/s41467-025-60920-0
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