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논문 기본 정보

자료유형
학술저널
저자정보
(Department of Immunology School of Basic Medicine Tongji Medical College Huazhong University of Sci) (Division of Pulmonary and Critical Care Medicine Department of Internal Medicine Tongji Hospital To) (Department of Immunology School of Basic Medicine Tongji Medical College Huazhong University of Sci) (Division of Pulmonary and Critical Care Medicine Department of Internal Medicine Tongji Hospital To) (Division of Pulmonary and Critical Care Medicine Department of Internal Medicine Tongji Hospital To) (Department of Immunology School of Basic Medicine Tongji Medical College Huazhong University of Sci) (Department of Immunology School of Basic Medicine Tongji Medical College Huazhong University of Sci) (Department of Immunology School of Basic Medicine Tongji Medical College Huazhong University of Sci) (Department of Surgery Tongji Hospital Huazhong University of Science and Technology (HUST) Wuhan Ch) (Department of Immunology School of Basic Medicine Tongji Medical College Huazhong University of Sci) (Laboratory of Cardiovascular Immunology Institute of Cardiology Union Hospital Tongji Medical Colle) (Department of Otolaryngology-Head and Neck Surgery Tongji Hospital Tongji Medical School Huazhong U) (University College Hospital NHS Trust London United Kingdom.) (Department of Otolaryngology Head and Neck Surgery Affiliated Eye-Ear-Nose and Throat Hospital Fuda) (Division of Pulmonary and Critical Care Medicine Department of Internal Medicine Tongji Hospital To) (Department of Immunology School of Basic Medicine Tongji Medical College Huazhong University of Sci)
저널정보
대한천식알레르기학회(구 대한알레르기학회) Allergy, Asthma & Immunology Research Allergy, Asthma & Immunology Research Vol.13 No.3
발행연도
수록면
479 - 497 (19page)

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초록· 키워드

Purpose Macrophages are important regulators of environmental allergen-induced airway inflammation and asthma. ATP6V0d2 is a subunit of vacuolar ATPase highly expressed in macrophages. However, the functions of ATP6V0d2 in the regulation of pathogenesis of allergic asthma remain unclear. The aim of this study is to determine the function and related molecular mechanisms of macrophage protein ATP6V0d2 in allergic asthma. Methods We compared the disease severity between female C57BL/6 wild-type and ATP6V0d2−/− mice in an ovalbumin (OVA)-induced asthma model. We also investigated the association of expression of ATP6V0d2, PU.1 and CCL17 with disease severity among asthmatic patients. Results The expression of ATP6V0d2 in sputum cells of asthmatic patients and in the lungs of OVA-challenged mice was enhanced compared to healthy subjects and their counterparts, respectively. However, ATP6V0d2-deficient mice exaggerated inflammatory cell infiltration as well as enhanced alternative activated macrophage (AAM) polarization and mucus production in an OVA-induced asthma model. Furthermore, we found that Atp6v0d2 promoted lysosomal degradation of Pu.1, which induced AAM polarization and Ccl17 production. Among asthma patients, ATP6V0d2 expression was inversely associated with disease severity, whereas PU.1 and CCL17 expression was positively associated with disease severity. Conclusions Our results identify macrophage Atp6v0d2, as an induced feedback inhibitor of asthma disease severity by promoting Pu.1 lysosomal degradation, which may in turn leads to reduced AAM polarization and Ccl17 production.
#Asthma #alveolar macrophage #V-type ATPase #Pu.1 protein
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