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

Joo Young Kim, Jung Ho Sohn, Jae Hyun Lee, Jungwon Park

Research output: Contribution to journalArticle

17 Citations (Scopus)

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 obesityrelated 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)-a 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 DIOOVA 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.

Original languageEnglish
Article numbere0116540
JournalPLoS One
Volume10
Issue number2
DOIs
Publication statusPublished - 2015 Feb 6

Fingerprint

tumor necrosis factors
Nutrition
obesity
Tumor Necrosis Factor-alpha
Obesity
asthma
Recovery
Asthma
Diet
mice
diet
Clodronic Acid
Alveolar Macrophages
Macrophages
Ovalbumin
Neutralizing Antibodies
Liposomes
exercise
macrophages
Immunoglobulin E

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)

Cite this

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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 obesityrelated 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)-a 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 DIOOVA 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.",
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Obesity increases airway hyperresponsiveness via the TNF-α pathway and treating obesity induces recovery. / Kim, Joo Young; Sohn, Jung Ho; Lee, Jae Hyun; Park, Jungwon.

In: PLoS One, Vol. 10, No. 2, e0116540, 06.02.2015.

Research output: Contribution to journalArticle

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