Effect of the anti-IL-17 antibody on allergic inflammation in an obesity-related asthma model.
- Author:
Lin LIANG
1
;
Jung HUR
;
Ji Young KANG
;
Chin Kook RHEE
;
Young Kyoon KIM
;
Sook Young LEE
Author Information
- Publication Type:Original Article
- Keywords: Asthma; Obesity; Anti-interleukin-7; Pravastatin; Inflammation
- MeSH: Adipokines; Adipose Tissue; Animals; Asthma*; Bronchoalveolar Lavage Fluid; Cell Differentiation; Diet, High-Fat; Goblet Cells; Humans; Inflammation*; Interleukin-17; Mice; Obesity; Ovalbumin; Ovum; Oxidoreductases; Pravastatin; Respiratory Hypersensitivity; Spleen
- From:The Korean Journal of Internal Medicine 2018;33(6):1210-1223
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND/AIMS: The co-occurrence of obesity aggravates asthma symptoms. Diet-induced obesity increases helper T cell (TH) 17 cell differentiation in adipose tissue and the spleen. The 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor pravastatin can potentially be used to treat asthma in obese patients by inhibiting interleukin 17 (IL-17) expression. This study investigated the combined effects of pravastatin and anti-IL-17 antibody treatment on allergic inflammation in a mouse model of obesity-related asthma. METHODS: High-fat diet (HFD)-induced obesity was induced in C57BL/6 mice with or without ovalbumin (OVA) sensitization and challenge. Mice were administered the anti-IL-17 antibody, pravastatin, or both, and pathophysiological and immunological responses were analyzed. RESULTS: HFD exacerbated allergic airway inflammation in the bronchoalveolar lavage fluid of HFD-OVA mice as compared to OVA mice. Blockading of the IL-17 in the HFD-OVA mice decreased airway hyper-responsiveness (AHR) and airway inflammation compared to the HFD-OVA mice. Moreover, the administration of the anti-IL-17 antibody decreased the leptin/adiponectin ratio in the HFD-OVA but not the OVA mice. Co-administration of pravastatin and anti-IL-17 inhibited airway inflammation and AHR, decreased goblet cell numbers, and increased adipokine levels in obese asthmatic mice. CONCLUSIONS: These results suggest that the IL-17–leptin/adiponectin axis plays a key role in airway inflammation in obesity-related asthma. Our findings suggest a potential new treatment for IL-17 as a target that may benefit obesity-related asthma patients who respond poorly to typical asthma medications.
