{"action":"create","ckan_id":null,"date_created":"Fri, 03 Apr 2026 23:26:22 GMT","date_finished":null,"harvest_job_id":"d7a0f2dc-d93b-461c-9c8a-75eefae341e6","harvest_source_id":"bebdce30-696c-424b-ad16-eca2913bde29","id":"218914ee-2181-49f5-ba0a-7b3b34bb3cc5","identifier":"https://data.cdc.gov/api/views/ef89-9ik2","parent_identifier":null,"source_hash":"9479b2fdf28a629973d7450d578fca4f76345e9709b4ba38a0ae7b8886395d83","source_raw":"{\"@type\": \"dcat:Dataset\", \"accessLevel\": \"public\", \"bureauCode\": [\"009:20\"], \"contactPoint\": {\"@type\": \"vcard:Contact\", \"fn\": \"Health Effects Laboratory Division, Pathology and Physiology Research Branch\", \"hasEmail\": \"mailto:sa-cin-webteam@cdc.gov\"}, \"description\": \"Interleukin (IL)-11, a pleiotropic, cationic cytokine, contributes to numerous biological processes, including adipogenesis, hematopoiesis, and inflammation.  Asthma, a chronic respiratory disease, is notably characterized by reversible airway obstruction, persistent lung inflammation, and airway hyperresponsiveness (AHR).  Nasal insufflation of IL-11 causes AHR in wild-type mice while lung inflammation induced by antigen sensitization and challenge, which mimics features of atopic asthma in humans, is attenuated in mice genetically deficient in IL-11 receptor subunit alpha-1 (IL-11R\\u03b11-deficient mice), a transmembrane receptor that is required along with glycoprotein 130 to transduce IL-11 intracellular signaling.  Nevertheless, the contribution of IL-11R\\u03b11 to the manifestation of phenotypic features of non-atopic asthma are not presently known. Thus, based on the aforementioned observations, we hypothesized that genetic deficiency of IL-11R\\u03b11 would attenuate lung inflammation and increases in airway responsiveness following acute inhalation exposure to ozone, a criteria pollutant and non-atopic asthma stimulus.\", \"distribution\": [{\"@type\": \"dcat:Distribution\", \"downloadURL\": \"https://data.cdc.gov/download/ef89-9ik2/application/x-zip-compressed\", \"mediaType\": \"application/x-zip-compressed\"}], \"identifier\": \"https://data.cdc.gov/api/views/ef89-9ik2\", \"issued\": \"2024-11-15\", \"landingPage\": \"https://data.cdc.gov/d/ef89-9ik2\", \"license\": \"http://opendefinition.org/licenses/odc-odbl/\", \"modified\": \"2026-01-14\", \"programCode\": [\"009:034\"], \"publisher\": {\"@type\": \"org:Organization\", \"name\": \"Centers for Disease Control and Prevention\"}, \"theme\": [\"National Institute for Occupational Safety and Health\"], \"title\": \"Interleukin-11 Receptor Subunit Alpha-1 is Required for Maximal Airway Responsiveness to Methacholine After Acute Exposure to Ozone\"}","source_transform":null,"status":"error"}