Adiponectin attenuates allergen-induced airway inflammation and hyperresponsiveness in mice
Epidemiologic data indicate an increased incidence of asthma in the obese. Because serum levels of the insulin-sensitizing and anti-inflammatory adipokine adiponectin are reduced in obese individuals, we sought to determine whether exogenous adiponectin can attenuate allergic airway responses. We se...
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| Published in | Journal of allergy and clinical immunology Vol. 118; no. 2; pp. 389 - 395 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York, NY
Mosby, Inc
01.08.2006
Elsevier Elsevier Limited |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0091-6749 1097-6825 |
| DOI | 10.1016/j.jaci.2006.04.021 |
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| Abstract | Epidemiologic data indicate an increased incidence of asthma in the obese.
Because serum levels of the insulin-sensitizing and anti-inflammatory adipokine adiponectin are reduced in obese individuals, we sought to determine whether exogenous adiponectin can attenuate allergic airway responses.
We sensitized and challenged BALB/cJ mice with ovalbumin (OVA). Alzet micro-osmotic pumps were implanted in the mice to deliver continuous infusions of buffer or adiponectin (1.0 μg/g/d), which resulted in an approximate 60% increase in serum adiponectin levels. Two days later, mice were challenged with aerosolized saline or OVA once per day for 3 days. Mice were examined 24 hours after the last challenge.
OVA challenge increased airway responsiveness to intravenous methacholine, bronchoalveolar lavage fluid cells, and T
H2 cytokine levels. Importantly, each of these responses to OVA was reduced in adiponectin- versus buffer-treated mice. OVA challenge caused a 30% reduction in serum adiponectin levels and a corresponding decrease in adipose tissue adiponectin mRNA expression. OVA challenge also decreased pulmonary mRNA expression of each of 3 proposed adiponectin-binding proteins, adiponectin receptor 1, adiponectin receptor 2, and T-cadherin.
Our results indicate that serum adiponectin is reduced during pulmonary allergic reactions and that adiponectin attenuates allergic airway inflammation and airway hyperresponsiveness in mice.
The data suggest that adiponectin might play a role in the relationship between obesity and asthma. |
|---|---|
| AbstractList | Background Epidemiologic data indicate an increased incidence of asthma in the obese. Objective Because serum levels of the insulin-sensitizing and anti-inflammatory adipokine adiponectin are reduced in obese individuals, we sought to determine whether exogenous adiponectin can attenuate allergic airway responses. Methods We sensitized and challenged BALB/cJ mice with ovalbumin (OVA). Alzet micro-osmotic pumps were implanted in the mice to deliver continuous infusions of buffer or adiponectin (1.0 μg/g/d), which resulted in an approximate 60% increase in serum adiponectin levels. Two days later, mice were challenged with aerosolized saline or OVA once per day for 3 days. Mice were examined 24 hours after the last challenge. Results OVA challenge increased airway responsiveness to intravenous methacholine, bronchoalveolar lavage fluid cells, and TH2 cytokine levels. Importantly, each of these responses to OVA was reduced in adiponectin- versus buffer-treated mice. OVA challenge caused a 30% reduction in serum adiponectin levels and a corresponding decrease in adipose tissue adiponectin mRNA expression. OVA challenge also decreased pulmonary mRNA expression of each of 3 proposed adiponectin-binding proteins, adiponectin receptor 1, adiponectin receptor 2, and T-cadherin. Conclusion Our results indicate that serum adiponectin is reduced during pulmonary allergic reactions and that adiponectin attenuates allergic airway inflammation and airway hyperresponsiveness in mice. Clinical implications The data suggest that adiponectin might play a role in the relationship between obesity and asthma. Epidemiologic data indicate an increased incidence of asthma in the obese. Because serum levels of the insulin-sensitizing and anti-inflammatory adipokine adiponectin are reduced in obese individuals, we sought to determine whether exogenous adiponectin can attenuate allergic airway responses. We sensitized and challenged BALB/cJ mice with ovalbumin (OVA). Alzet micro-osmotic pumps were implanted in the mice to deliver continuous infusions of buffer or adiponectin (1.0 μg/g/d), which resulted in an approximate 60% increase in serum adiponectin levels. Two days later, mice were challenged with aerosolized saline or OVA once per day for 3 days. Mice were examined 24 hours after the last challenge. OVA challenge increased airway responsiveness to intravenous methacholine, bronchoalveolar lavage fluid cells, and T H2 cytokine levels. Importantly, each of these responses to OVA was reduced in adiponectin- versus buffer-treated mice. OVA challenge caused a 30% reduction in serum adiponectin levels and a corresponding decrease in adipose tissue adiponectin mRNA expression. OVA challenge also decreased pulmonary mRNA expression of each of 3 proposed adiponectin-binding proteins, adiponectin receptor 1, adiponectin receptor 2, and T-cadherin. Our results indicate that serum adiponectin is reduced during pulmonary allergic reactions and that adiponectin attenuates allergic airway inflammation and airway hyperresponsiveness in mice. The data suggest that adiponectin might play a role in the relationship between obesity and asthma. Epidemiologic data indicate an increased incidence of asthma in the obese.BACKGROUNDEpidemiologic data indicate an increased incidence of asthma in the obese.Because serum levels of the insulin-sensitizing and anti-inflammatory adipokine adiponectin are reduced in obese individuals, we sought to determine whether exogenous adiponectin can attenuate allergic airway responses.OBJECTIVEBecause serum levels of the insulin-sensitizing and anti-inflammatory adipokine adiponectin are reduced in obese individuals, we sought to determine whether exogenous adiponectin can attenuate allergic airway responses.We sensitized and challenged BALB/cJ mice with ovalbumin (OVA). Alzet micro-osmotic pumps were implanted in the mice to deliver continuous infusions of buffer or adiponectin (1.0 microg/g/d), which resulted in an approximate 60% increase in serum adiponectin levels. Two days later, mice were challenged with aerosolized saline or OVA once per day for 3 days. Mice were examined 24 hours after the last challenge.METHODSWe sensitized and challenged BALB/cJ mice with ovalbumin (OVA). Alzet micro-osmotic pumps were implanted in the mice to deliver continuous infusions of buffer or adiponectin (1.0 microg/g/d), which resulted in an approximate 60% increase in serum adiponectin levels. Two days later, mice were challenged with aerosolized saline or OVA once per day for 3 days. Mice were examined 24 hours after the last challenge.OVA challenge increased airway responsiveness to intravenous methacholine, bronchoalveolar lavage fluid cells, and T(H)2 cytokine levels. Importantly, each of these responses to OVA was reduced in adiponectin- versus buffer-treated mice. OVA challenge caused a 30% reduction in serum adiponectin levels and a corresponding decrease in adipose tissue adiponectin mRNA expression. OVA challenge also decreased pulmonary mRNA expression of each of 3 proposed adiponectin-binding proteins, adiponectin receptor 1, adiponectin receptor 2, and T-cadherin.RESULTSOVA challenge increased airway responsiveness to intravenous methacholine, bronchoalveolar lavage fluid cells, and T(H)2 cytokine levels. Importantly, each of these responses to OVA was reduced in adiponectin- versus buffer-treated mice. OVA challenge caused a 30% reduction in serum adiponectin levels and a corresponding decrease in adipose tissue adiponectin mRNA expression. OVA challenge also decreased pulmonary mRNA expression of each of 3 proposed adiponectin-binding proteins, adiponectin receptor 1, adiponectin receptor 2, and T-cadherin.Our results indicate that serum adiponectin is reduced during pulmonary allergic reactions and that adiponectin attenuates allergic airway inflammation and airway hyperresponsiveness in mice.CONCLUSIONOur results indicate that serum adiponectin is reduced during pulmonary allergic reactions and that adiponectin attenuates allergic airway inflammation and airway hyperresponsiveness in mice.The data suggest that adiponectin might play a role in the relationship between obesity and asthma.CLINICAL IMPLICATIONSThe data suggest that adiponectin might play a role in the relationship between obesity and asthma. Epidemiologic data indicate an increased incidence of asthma in the obese. Because serum levels of the insulin-sensitizing and anti-inflammatory adipokine adiponectin are reduced in obese individuals, we sought to determine whether exogenous adiponectin can attenuate allergic airway responses. We sensitized and challenged BALB/cJ mice with ovalbumin (OVA). Alzet micro-osmotic pumps were implanted in the mice to deliver continuous infusions of buffer or adiponectin (1.0 microg/g/d), which resulted in an approximate 60% increase in serum adiponectin levels. Two days later, mice were challenged with aerosolized saline or OVA once per day for 3 days. Mice were examined 24 hours after the last challenge. OVA challenge increased airway responsiveness to intravenous methacholine, bronchoalveolar lavage fluid cells, and T(H)2 cytokine levels. Importantly, each of these responses to OVA was reduced in adiponectin- versus buffer-treated mice. OVA challenge caused a 30% reduction in serum adiponectin levels and a corresponding decrease in adipose tissue adiponectin mRNA expression. OVA challenge also decreased pulmonary mRNA expression of each of 3 proposed adiponectin-binding proteins, adiponectin receptor 1, adiponectin receptor 2, and T-cadherin. Our results indicate that serum adiponectin is reduced during pulmonary allergic reactions and that adiponectin attenuates allergic airway inflammation and airway hyperresponsiveness in mice. The data suggest that adiponectin might play a role in the relationship between obesity and asthma. |
| Author | Hug, Christopher Shore, Stephanie A. Terry, Raya D. Xu, Aimin Flynt, Lesley |
| Author_xml | – sequence: 1 givenname: Stephanie A. surname: Shore fullname: Shore, Stephanie A. email: sshore@hsph.harvard.edu organization: From the Physiology Program, Department of Environmental Health, Harvard School of Public Health, Boston – sequence: 2 givenname: Raya D. surname: Terry fullname: Terry, Raya D. organization: From the Physiology Program, Department of Environmental Health, Harvard School of Public Health, Boston – sequence: 3 givenname: Lesley surname: Flynt fullname: Flynt, Lesley organization: From the Physiology Program, Department of Environmental Health, Harvard School of Public Health, Boston – sequence: 4 givenname: Aimin surname: Xu fullname: Xu, Aimin organization: Department of Medicine, University of Hong Kong – sequence: 5 givenname: Christopher surname: Hug fullname: Hug, Christopher organization: Pulmonary Division, Children's Hospital, Boston |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18028066$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/16890763$$D View this record in MEDLINE/PubMed |
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| Keywords | airway responsiveness adiponectin receptor 1 adiponectin receptor 2 TBS Lung IgE BALF IL-5 IL-13 BAL AdipoR2 AdipoR1 NF-κB T-cadherin adipocyte OVA eosinophil R L Adipocyte Allergy Hyperreactivity Granulocyte Respiratory system Adiponectin Respiratory tract Immunology Interleukin 5 Immunopathology Cytokine Rodentia Adiponectin Receptor 1 Inflammation Interleukin 13 Cadherin Eosinophil Adiponectin Receptor 2 Vertebrata Mammalia Mouse Animal Allergen |
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| Snippet | Epidemiologic data indicate an increased incidence of asthma in the obese.
Because serum levels of the insulin-sensitizing and anti-inflammatory adipokine... Background Epidemiologic data indicate an increased incidence of asthma in the obese. Objective Because serum levels of the insulin-sensitizing and... Epidemiologic data indicate an increased incidence of asthma in the obese.BACKGROUNDEpidemiologic data indicate an increased incidence of asthma in the... |
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| SubjectTerms | adipocyte Adipocytes Adiponectin - blood Adiponectin - genetics Adiponectin - pharmacology adiponectin receptor 1 adiponectin receptor 2 Adipose Tissue - drug effects Adipose Tissue - metabolism airway responsiveness Allergens - pharmacology Animals Biological and medical sciences Bronchial Hyperreactivity - immunology Bronchial Hyperreactivity - prevention & control Bronchoalveolar Lavage Fluid - cytology Bronchoalveolar Lavage Fluid - immunology Cadherins - genetics Cadherins - metabolism eosinophil Female Fundamental and applied biological sciences. Psychology Fundamental immunology Gene expression Gene Expression Regulation - drug effects Human subjects IgE IL-13 IL-5 Immunoglobulin E - blood Immunopathology Leukocytes - drug effects Lung Lung - drug effects Lung - physiology Lungs Male Medical sciences Mice Mice, Inbred BALB C Obesity Ovalbumin - pharmacology Pneumonia - immunology Pneumonia - prevention & control Protein expression Receptors, Adiponectin Receptors, Cell Surface - genetics Receptors, Cell Surface - metabolism Recombinant Proteins - pharmacology RNA, Messenger - biosynthesis Rodents T-cadherin Weight control |
| Title | Adiponectin attenuates allergen-induced airway inflammation and hyperresponsiveness in mice |
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