Obesity enhances eosinophilic inflammation in a murine model of allergic asthma

Background and purpose:  Obesity is associated with deterioration in asthma outcomes. Although airways eosinophil accumulation is characteristic of lung allergic diseases, little is known about the influence of obesity on the allergic eosinophil trafficking from bone marrow to lung tissues, and recr...

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Bibliographic Details
Published in:British journal of pharmacology 2010-02, Vol.159 (3), p.617-625
Main Authors: Calixto, MC, Lintomen, L, Schenka, A, Saad, MJ, Zanesco, A, Antunes, E
Format: Article
Language:English
Subjects:
Animals
asthma
Asthma - immunology
Asthma - pathology
Biological and medical sciences
Bone marrow
Bone Marrow - immunology
Bronchi - immunology
Bronchoalveolar Lavage Fluid - immunology
Chemokine CCL11
Chronic obstructive pulmonary disease, asthma
Cytokines
Cytokines - biosynthesis
Cytokines - immunology
Cytokines - pharmacology
eosinophil
Eosinophilia - immunology
Eosinophilia - pathology
Eosinophils - immunology
eotaxin
Hypersensitivity - immunology
Hypersensitivity - pathology
Inflammation - immunology
Inflammation - pathology
Interleukin-10 - immunology
Interleukin-10 - pharmacology
Interleukin-5 - immunology
Interleukin-5 - pharmacology
Lung - drug effects
Lung - immunology
Lung - pathology
Lung Diseases - immunology
Lung Diseases - pathology
Male
Medical sciences
Metabolic diseases
Mice
Mice, Inbred C57BL
Obesity
Obesity - immunology
Obesity - pathology
Ovalbumin - immunology
Ovalbumin - pharmacology
Pharmacology. Drug treatments
Pneumology
Pneumonia - immunology
Pneumonia - pathology
Research Papers
TH2 cytokines
Tumor Necrosis Factor-alpha - immunology
Tumor Necrosis Factor-alpha - pharmacology
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Summary:Background and purpose:  Obesity is associated with deterioration in asthma outcomes. Although airways eosinophil accumulation is characteristic of lung allergic diseases, little is known about the influence of obesity on the allergic eosinophil trafficking from bone marrow to lung tissues, and recruitment to airways lumen. Here, we have assessed the effects of diet‐induced obesity on allergic eosinophilic inflammation in mice, examining eosinophil trafficking from bone marrow to airways, and production of TH1/TH2 cytokines. Experimental approach:  C57BL/6 mice fed for 10 weeks with standard chow or high‐fat diet were sensitized and challenged with ovalbumin. At 24–96 h post‐ovalbumin challenge, bronchoalveolar lavage (BAL) fluid, lung tissue and bone marrow were examined. Key results:  The high‐fat‐fed mice exhibited increased body weight and epididymal fat, glucose intolerance and alterations in lipid profile compared with the lean mice. Obesity markedly elevated serum leptin and lowered adiponectin levels. Ovalbumin challenge in obese mice promoted a markedly higher eosinophil accumulation in bone marrow and connective tissue surrounding the bronchial and bronchiolar segments. Eosinophil number in BAL fluid of obese mice was lower at 24 and 48 h. Levels of interleukin (IL)‐5, eotaxin, tumour necrosis factor‐α and IL‐10 in BAL fluid of obese mice were significantly higher than in lean mice. Conclusions and implications:  Diet‐induced obesity enhanced eosinophil trafficking from bone marrow to lung tissues, and delayed their transit through the airway epithelium into the airway lumen. Consequently, eosinophils remain longer in lung peribronchiolar segments due to overproduction of TH1/TH2 cytokines and chemokines.
ISSN:0007-1188
1476-5381
DOI:10.1111/j.1476-5381.2009.00560.x