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National Institute of Environmental Health Sciences

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Your Environment. Your Health.

Publication Detail

Title: Pulmonary inflammation induced by subacute ozone is augmented in adiponectin-deficient mice: role of IL-17A.

Authors: Kasahara, David I; Kim, Hye Y; Williams, Alison S; Verbout, Norah G; Tran, Jennifer; Si, Huiqing; Wurmbrand, Allison P; Jastrab, Jordan; Hug, Christopher; Umetsu, Dale T; Shore, Stephanie A

Published In J Immunol, (2012 May 1)

Abstract: Pulmonary responses to ozone, a common air pollutant, are augmented in obese individuals. Adiponectin, an adipose-derived hormone that declines in obesity, has regulatory effects on the immune system. To determine the role of adiponectin in the pulmonary inflammation induced by extended (48-72 h) low-dose (0.3 parts per million) exposure to ozone, adiponectin-deficient (Adipo(-/-)) and wild-type mice were exposed to ozone or to room air. In wild-type mice, ozone exposure increased total bronchoalveolar lavage (BAL) adiponectin. Ozone-induced lung inflammation, including increases in BAL neutrophils, protein (an index of lung injury), IL-6, keratinocyte-derived chemokine, LPS-induced CXC chemokine, and G-CSF were augmented in Adipo(-/-) versus wild-type mice. Ozone also increased IL-17A mRNA expression to a greater extent in Adipo(-/-) versus wild-type mice. Moreover, compared with control Ab, anti-IL-17A Ab attenuated ozone-induced increases in BAL neutrophils and G-CSF in Adipo(-/-) but not in wild-type mice, suggesting that IL-17A, by promoting G-CSF release, contributed to augmented neutrophilia in Adipo(-/-) mice. Flow cytometric analysis of lung cells revealed that the number of CD45(+)/F4/80(+)/IL-17A(+) macrophages and ýýýý T cells expressing IL-17A increased after ozone exposure in wild-type mice and further increased in Adipo(-/-) mice. The IL-17(+) macrophages were CD11c(-) (interstitial macrophages), whereas CD11c(+) macrophages (alveolar macrophages) did not express IL-17A. Taken together, the data are consistent with the hypothesis that adiponectin protects against neutrophil recruitment induced by extended low-dose ozone exposure by inhibiting the induction and/or recruitment of IL-17A in interstitial macrophages and/or ýýýý T cells.

PubMed ID: 22474022 Exiting the NIEHS site

MeSH Terms: Adiponectin/genetics; Adiponectin/immunology*; Adiponectin/metabolism; Animals; Antigens, Differentiation/genetics; Antigens, Differentiation/immunology; Antigens, Differentiation/metabolism; Bronchoalveolar Lavage; Cytokines/genetics; Cytokines/immunology; Cytokines/metabolism; Dose-Response Relationship, Drug; Interleukin-17/genetics; Interleukin-17/immunology*; Interleukin-17/metabolism; Lipopolysaccharides/pharmacology; Macrophages, Alveolar/immunology*; Macrophages, Alveolar/metabolism; Macrophages, Alveolar/pathology; Mice; Mice, Knockout; Neutrophils/immunology*; Neutrophils/metabolism; Neutrophils/pathology; Oxidants, Photochemical/adverse effects*; Oxidants, Photochemical/pharmacology; Ozone/adverse effects*; Ozone/pharmacology; Pneumonia/chemically induced; Pneumonia/genetics; Pneumonia/immunology*; Pneumonia/metabolism; Pneumonia/pathology; Receptors, Antigen, T-Cell, gamma-delta/genetics; Receptors, Antigen, T-Cell, gamma-delta/immunology; Receptors, Antigen, T-Cell, gamma-delta/metabolism; T-Lymphocytes/immunology; T-Lymphocytes/metabolism; T-Lymphocytes/pathology

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