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http://purl.uniprot.org/citations/26386120http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26386120http://www.w3.org/2000/01/rdf-schema#comment"Acute exposure to ozone (O3), an air pollutant, causes pulmonary inflammation, airway epithelial desquamation, and airway hyperresponsiveness (AHR). Pro-inflammatory cytokines-including IL-6 and ligands of chemokine (C-X-C motif) receptor 2 [keratinocyte chemoattractant (KC) and macrophage inflammatory protein (MIP)-2], TNF receptor 1 and 2 (TNF), and type I IL-1 receptor (IL-1α and IL-1β)-promote these sequelae. Human resistin, a pleiotropic hormone and cytokine, induces expression of IL-1α, IL-1β, IL-6, IL-8 (the human ortholog of murine KC and MIP-2), and TNF. Functional differences exist between human and murine resistin; yet given the aforementioned observations, we hypothesized that murine resistin promotes O3-induced lung pathology by inducing expression of the same inflammatory cytokines as human resistin. Consequently, we examined indexes of O3-induced lung pathology in wild-type and resistin-deficient mice following acute exposure to either filtered room air or O3. In wild-type mice, O3 increased bronchoalveolar lavage fluid (BALF) resistin. Furthermore, O3 increased lung tissue or BALF IL-1α, IL-6, KC, TNF, macrophages, neutrophils, and epithelial cells in wild-type and resistin-deficient mice. With the exception of KC, which was significantly greater in resistin-deficient compared with wild-type mice, no genotype-related differences in the other indexes existed following O3 exposure. O3 caused AHR to acetyl-β-methylcholine chloride (methacholine) in wild-type and resistin-deficient mice. However, genotype-related differences in airway responsiveness to methacholine were nonexistent subsequent to O3 exposure. Taken together, these data demonstrate that murine resistin is increased in the lungs of wild-type mice following acute O3 exposure but does not promote O3-induced lung pathology."xsd:string
http://purl.uniprot.org/citations/26386120http://purl.org/dc/terms/identifier"doi:10.1152/ajplung.00270.2015"xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/author"Blackburn M.R."xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/author"Malik F."xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/author"Alexander A.L."xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/author"Price R.E."xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/author"Weng T."xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/author"Johnston R.A."xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/author"Richards J.B."xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/author"Atkins C.L."xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/author"Alcorn J.L."xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/author"Haque I.U."xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/author"Cromar K.R."xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/author"Spencer C.Y."xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/author"Bell C.S."xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/author"Cockerill K.J."xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/author"Razvi S.S."xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/name"Am J Physiol Lung Cell Mol Physiol"xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/pages"L1174-85"xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/title"Resistin deficiency in mice has no effect on pulmonary responses induced by acute ozone exposure."xsd:string
http://purl.uniprot.org/citations/26386120http://purl.uniprot.org/core/volume"309"xsd:string
http://purl.uniprot.org/citations/26386120http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/26386120
http://purl.uniprot.org/citations/26386120http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/26386120