Obesity enhances eosinophilic inflammation in a murine model of allergic asthma
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Data
2010-02-01
Autores
Calixto, M. C.
Lintomen, L.
Schenka, A.
Saad, M. J.
Zanesco, A. [UNESP]
Antunes, E.
Título da Revista
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Título de Volume
Editor
Wiley-Blackwell Publishing, Inc
Resumo
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 T(H)1/T(H)2 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-alpha 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 T(H)1/T(H)2 cytokines and chemokines.
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Palavras-chave
obesity, asthma, eosinophil, bone marrow, eotaxin, T(H)2 cytokines
Como citar
British Journal of Pharmacology. Malden: Wiley-blackwell Publishing, Inc, v. 159, n. 3, p. 617-625, 2010.