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dc.contributor.author김주영-
dc.date.accessioned2016-08-27T04:08:11Z-
dc.date.available2016-08-27T04:08:11Z-
dc.date.issued2015-
dc.identifier.issn1932-6203-
dc.identifier.otherOAK-14590-
dc.identifier.urihttps://dspace.ewha.ac.kr/handle/2015.oak/217019-
dc.description.abstractObesity is a known risk factor for allergic asthma. It has been recognized as a key player in the pathogenesis of several inflammatory disorders via activation of macrophages, which is also vital to the development of allergic asthma. We investigated the mechanism of obesity-related asthma and whether treating obesity through exercise or diet ameliorates the severity of asthma in the obesity-related asthma model. We generated diet-induced obesity (DIO) in C57BL/6 mice by high-fat-feeding and ovalbumin-induced asthma (lean-OVA or DIOOVA). The DIO-OVA mice were then treated with tumor necrosis factor (TNF)-alpha neutralizing antibody as a TNF-alpha blockade or a Cl2MDP-containing liposome to induce an alveolar macrophage deficiency. To treat obesity, the DIO-OVA mice were under dietary restrictions or exercised. The pathophysiological and immunological responses were analyzed. Airway hyperresponsiveness (AHR), serum IgE and TNF-alpha levels in the lung tissue increased in the DIO-OVA mice compared to the lean-OVA mice. Both the TNF-alpha blockade and depletion of alveolar macrophages in the DIO-OVA mice decreased AHR compared to the DIOOVA mice. Treating obesity by exercise or through dietary means also reduced pulmonary TNF-alpha levels and AHR in the DIO-OVA mice. These results suggest that restoring normal body weight is an appropriate strategy for reducing TNF-alpha levels, and controlling inflammation may help improve asthma severity and control in obesity-related asthma.-
dc.languageEnglish-
dc.publisherPUBLIC LIBRARY SCIENCE-
dc.titleObesity Increases Airway Hyperresponsiveness via the TNF-alpha Pathway and Treating Obesity Induces Recovery-
dc.typeArticle-
dc.relation.issue2-
dc.relation.volume10-
dc.relation.indexSCIE-
dc.relation.indexSCOPUS-
dc.relation.journaltitlePLOS ONE-
dc.identifier.doi10.1371/journal.pone.0116540-
dc.identifier.wosidWOS:000349444900047-
dc.author.googleKim, Joo Young-
dc.author.googleSohn, Jung-Ho-
dc.author.googleLee, Jae-Hyun-
dc.author.googlePark, Jung-Won-
dc.contributor.scopusid김주영(54789010200;57221537444)-
dc.date.modifydate20220112111641-


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