Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 조영주 | * |
dc.contributor.author | 김민혜 | * |
dc.contributor.author | 심지수 | * |
dc.date.accessioned | 2023-07-31T16:31:22Z | - |
dc.date.available | 2023-07-31T16:31:22Z | - |
dc.date.issued | 2023 | * |
dc.identifier.issn | 1040-0605 | * |
dc.identifier.other | OAK-33452 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/265388 | - |
dc.description.abstract | In obesity, disturbed glutamine metabolism contributes to enhanced inflammation by inducing alterations in immune cells. As macrophages and innate lymphoid cells (ILCs) are known to be involved in the pathogenesis of obesity-related asthma, we tested our hypothesis that altered glutamine metabolism may link obesity to airway hyperresponsivenss (AHR), a cardinal feature of asthma, focusing on these innate immune cells. Four-week-old male C57BL/6 mice were fed a high-fat diet (HFD) for 13 wk in the presence or absence of BPTES [Bis-2-(5-phenylacetamido-1,3,4-thiadiazol-2-yl)ethyl sulfide, a selective inhibitor of glutaminase 1 which converts glutamine to glutamate] and their blood, lung, and adipose tissues were analyzed. We then conducted in vitro experiments using bone marrow-derived macrophages (BMDMs) and mouse alveolar macrophage cell line. Furthermore, we investigated plasma glutamine and glutamate levels in obese and nonobese asthmatics. BPTES treatment prevented HFD-induced AHR and significantly decreased IL-1β+ classically activated macrophages (M1s) and type 3 ILCs (ILC3s) which increased in the lungs of HFD-fed obese mice. In in vitro experiments, BPTES treatment or glutamine supplement significantly reduced the proportion of IL-1β+NLRP3+ M1s in lipopolysaccharide-stimulated BMDMs and mouse alveolar macrophage cell line. BPTES treatment also significantly reduced the IL-17 producing ILC3s differentiated from ILCs in naïve mouse lung. In addition, plasma glutamate/glutamine ratios were significantly higher in obese asthmatics compared to nonobese asthmatics. Inhibition of glutaminolysis reverses AHR in HFD-induced obese mice and decreases IL-1β + NLRP3+ M1s and IL-17 producing ILC3s, which suggests altered glutamine metabolism may have a role in the pathogenesis of obesity-related AHR. Copyright © 2023 the American Physiological Society. | * |
dc.language | English | * |
dc.publisher | American Physiological Society | * |
dc.subject | asthma | * |
dc.subject | glutamine | * |
dc.subject | innate lymphoid cells | * |
dc.subject | macrophages | * |
dc.subject | obesity | * |
dc.title | Inhibition of glutaminase 1 activity reverses airway hyperresponsiveness and decreases IL-1β+ M1s and IL-17 producing ILC3s in high-fat diet-fed obese mice | * |
dc.type | Article | * |
dc.relation.issue | 5 | * |
dc.relation.volume | 324 | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | L625 | * |
dc.relation.lastpage | L638 | * |
dc.relation.journaltitle | American Journal of Physiology - Lung Cellular and Molecular Physiology | * |
dc.identifier.doi | 10.1152/ajplung.00181.2022 | * |
dc.identifier.wosid | WOS:000981682600002 | * |
dc.identifier.scopusid | 2-s2.0-85152600840 | * |
dc.author.google | Shim J.-S. | * |
dc.author.google | Lee H.-S. | * |
dc.author.google | Kwon H. | * |
dc.author.google | Kim M.-H. | * |
dc.author.google | Cho Y.-J. | * |
dc.author.google | Park H.-W. | * |
dc.contributor.scopusid | 조영주(55472202600;56657140200) | * |
dc.contributor.scopusid | 김민혜(58045929900) | * |
dc.contributor.scopusid | 심지수(57193221759) | * |
dc.date.modifydate | 20240315131743 | * |