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 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. RESULTS: 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. 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.
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 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. RESULTS: 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. 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.
Authors: Akshay Sood; Clifford Qualls; Mark Schuyler; Bharat Thyagarajan; Michael W Steffes; Lewis J Smith; David R Jacobs Journal: Am J Respir Crit Care Med Date: 2012-04-06 Impact factor: 21.405
Authors: Fredrick J Rosario; Michael A Schumacher; Jean Jiang; Yoshikatsu Kanai; Theresa L Powell; Thomas Jansson Journal: J Physiol Date: 2012-01-30 Impact factor: 5.182
Authors: Ming Zhu; Christopher Hug; David I Kasahara; Richard A Johnston; Alison S Williams; Norah G Verbout; Huiqing Si; Jordan Jastrab; Amit Srivastava; Erin S Williams; Barbara Ranscht; Stephanie A Shore Journal: Am J Respir Cell Mol Biol Date: 2009-11-13 Impact factor: 6.914