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Cited 47 times in

Obesity increases airway hyperresponsiveness via the TNF-α pathway and treating obesity induces recovery

DC Field Value Language
dc.contributor.author박중원-
dc.contributor.author손정호-
dc.contributor.author이재현-
dc.date.accessioned2016-02-04T11:05:20Z-
dc.date.available2016-02-04T11:05:20Z-
dc.date.issued2015-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/139637-
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 DIO-OVA). The DIO-OVA mice were then treated with tumor necrosis factor (TNF)-α neutralizing antibody as a TNF-α 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-α levels in the lung tissue increased in the DIO-OVA mice compared to the lean-OVA mice. Both the TNF-α blockade and depletion of alveolar macrophages in the DIO-OVA mice decreased AHR compared to the DIO-OVA mice. Treating obesity by exercise or through dietary means also reduced pulmonary TNF-α levels and AHR in the DIO-OVA mice. These results suggest that restoring normal body weight is an appropriate strategy for reducing TNF-α levels, and controlling inflammation may help improve asthma severity and control in obesity-related asthma.-
dc.description.statementOfResponsibilityopen-
dc.format.extente0116540-
dc.relation.isPartOfPLOS ONE-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHAntibodies, Neutralizing/administration & dosage*-
dc.subject.MESHAntibodies, Neutralizing/adverse effects-
dc.subject.MESHBody Weight/drug effects-
dc.subject.MESHClodronic Acid/administration & dosage*-
dc.subject.MESHDiet Therapy-
dc.subject.MESHDiet, High-Fat-
dc.subject.MESHDisease Models, Animal-
dc.subject.MESHExercise Therapy-
dc.subject.MESHMacrophages, Alveolar/drug effects-
dc.subject.MESHMacrophages, Alveolar/pathology-
dc.subject.MESHMice-
dc.subject.MESHObesity/complications-
dc.subject.MESHObesity/etiology-
dc.subject.MESHObesity/physiopathology-
dc.subject.MESHObesity/therapy*-
dc.subject.MESHOvalbumin-
dc.subject.MESHRespiratory Hypersensitivity/chemically induced-
dc.subject.MESHRespiratory Hypersensitivity/drug therapy*-
dc.subject.MESHRespiratory Hypersensitivity/immunology-
dc.subject.MESHTumor Necrosis Factor-alpha/antagonists & inhibitors*-
dc.subject.MESHTumor Necrosis Factor-alpha/metabolism-
dc.titleObesity increases airway hyperresponsiveness via the TNF-α pathway and treating obesity induces recovery-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorJoo Young Kim-
dc.contributor.googleauthorJung-Ho Sohn-
dc.contributor.googleauthorJae-Hyun Lee-
dc.contributor.googleauthorJung-Won Park-
dc.identifier.doi10.1371/journal.pone.0116540-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01681-
dc.contributor.localIdA01993-
dc.contributor.localIdA03086-
dc.relation.journalcodeJ02540-
dc.identifier.eissn1932-6203-
dc.identifier.pmid25658739-
dc.contributor.alternativeNamePark, Jung Won-
dc.contributor.alternativeNameSohn, Jung Ho-
dc.contributor.alternativeNameLee, Jae Hyun-
dc.contributor.affiliatedAuthorPark, Jung Won-
dc.contributor.affiliatedAuthorSohn, Jung Ho-
dc.contributor.affiliatedAuthorLee, Jae Hyun-
dc.rights.accessRightsfree-
dc.citation.volume10-
dc.citation.number2-
dc.citation.startPagee0116540-
dc.identifier.bibliographicCitationPLOS ONE, Vol.10(2) : e0116540, 2015-
dc.identifier.rimsid52375-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers

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