The adipocyte fatty acid-binding protein aP2 is required in allergic airway inflammation
| Autor: | Charles R. Mackay, Melinda J Frost, Cem Z. Görgün, Bennett O.V. Shum, Rakesh K. Kumar, G S Hotamisligil, Michael S. Rolph |
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| Rok vydání: | 2006 |
| Předmět: |
Transcription
Genetic T cell Cell Culture Techniques Bronchi Inflammation Respiratory Mucosa Biology Fatty Acid-Binding Proteins Allergic inflammation Mice chemistry.chemical_compound Th2 Cells Adipocyte Adipocytes Hypersensitivity medicine Animals RNA Messenger Interleukin 4 Mice Knockout Fatty acid metabolism Fatty Acids food and beverages Lipid metabolism 3T3 Cells General Medicine respiratory system Interleukin-12 Asthma respiratory tract diseases Disease Models Animal medicine.anatomical_structure chemistry Immunology Interleukin 12 Interleukin-4 medicine.symptom Research Article |
| Zdroj: | Journal of Clinical Investigation. 116:2183-2192 |
| ISSN: | 0021-9738 |
| Popis: | The adipocyte fatty acid–binding protein aP2 regulates systemic glucose and lipid metabolism. We report that aP2, in addition to being abundantly expressed by adipocytes, is also expressed by human airway epithelial cells and shows a striking upregulation following stimulation of epithelial cells with the Th2 cytokines IL-4 and IL-13. Regulation of aP2 mRNA expression by Th2 cytokines was highly dependent on STAT6, a transcription factor with a major regulatory role in allergic inflammation. We examined aP2-deficient mice in a model of allergic airway inflammation and found that infiltration of leukocytes, especially eosinophils, into the airways was highly dependent on aP2 function. T cell priming was unaffected by aP2 deficiency, suggesting that aP2 was acting locally within the lung, and analysis of bone marrow chimeras implicated non-hematopoietic cells, most likely bronchial epithelial cells, as the site of action of aP2 in allergic airway inflammation. Thus, aP2 regulates allergic airway inflammation and may provide a link between fatty acid metabolism and asthma. |
| Databáze: | OpenAIRE |
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