Cited 47 times in
Obesity increases airway hyperresponsiveness via the TNF-α pathway and treating obesity induces recovery
DC Field | Value | Language |
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dc.contributor.author | 박중원 | - |
dc.contributor.author | 손정호 | - |
dc.contributor.author | 이재현 | - |
dc.date.accessioned | 2016-02-04T11:05:20Z | - |
dc.date.available | 2016-02-04T11:05:20Z | - |
dc.date.issued | 2015 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/139637 | - |
dc.description.abstract | Obesity 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.statementOfResponsibility | open | - |
dc.format.extent | e0116540 | - |
dc.relation.isPartOf | PLOS ONE | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Antibodies, Neutralizing/administration & dosage* | - |
dc.subject.MESH | Antibodies, Neutralizing/adverse effects | - |
dc.subject.MESH | Body Weight/drug effects | - |
dc.subject.MESH | Clodronic Acid/administration & dosage* | - |
dc.subject.MESH | Diet Therapy | - |
dc.subject.MESH | Diet, High-Fat | - |
dc.subject.MESH | Disease Models, Animal | - |
dc.subject.MESH | Exercise Therapy | - |
dc.subject.MESH | Macrophages, Alveolar/drug effects | - |
dc.subject.MESH | Macrophages, Alveolar/pathology | - |
dc.subject.MESH | Mice | - |
dc.subject.MESH | Obesity/complications | - |
dc.subject.MESH | Obesity/etiology | - |
dc.subject.MESH | Obesity/physiopathology | - |
dc.subject.MESH | Obesity/therapy* | - |
dc.subject.MESH | Ovalbumin | - |
dc.subject.MESH | Respiratory Hypersensitivity/chemically induced | - |
dc.subject.MESH | Respiratory Hypersensitivity/drug therapy* | - |
dc.subject.MESH | Respiratory Hypersensitivity/immunology | - |
dc.subject.MESH | Tumor Necrosis Factor-alpha/antagonists & inhibitors* | - |
dc.subject.MESH | Tumor Necrosis Factor-alpha/metabolism | - |
dc.title | Obesity increases airway hyperresponsiveness via the TNF-α pathway and treating obesity induces recovery | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Internal Medicine (내과학) | - |
dc.contributor.googleauthor | Joo Young Kim | - |
dc.contributor.googleauthor | Jung-Ho Sohn | - |
dc.contributor.googleauthor | Jae-Hyun Lee | - |
dc.contributor.googleauthor | Jung-Won Park | - |
dc.identifier.doi | 10.1371/journal.pone.0116540 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A01681 | - |
dc.contributor.localId | A01993 | - |
dc.contributor.localId | A03086 | - |
dc.relation.journalcode | J02540 | - |
dc.identifier.eissn | 1932-6203 | - |
dc.identifier.pmid | 25658739 | - |
dc.contributor.alternativeName | Park, Jung Won | - |
dc.contributor.alternativeName | Sohn, Jung Ho | - |
dc.contributor.alternativeName | Lee, Jae Hyun | - |
dc.contributor.affiliatedAuthor | Park, Jung Won | - |
dc.contributor.affiliatedAuthor | Sohn, Jung Ho | - |
dc.contributor.affiliatedAuthor | Lee, Jae Hyun | - |
dc.rights.accessRights | free | - |
dc.citation.volume | 10 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | e0116540 | - |
dc.identifier.bibliographicCitation | PLOS ONE, Vol.10(2) : e0116540, 2015 | - |
dc.identifier.rimsid | 52375 | - |
dc.type.rims | ART | - |
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