{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T14:23:50Z","timestamp":1791037430792,"version":"4.1.0"},"reference-count":41,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2000,11,1]],"date-time":"2000-11-01T00:00:00Z","timestamp":973036800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2000,11,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The relationship between eosinophils and the development of Ag-induced pulmonary pathologies, including airway hyper-responsiveness, was investigated using mice deficient for the secondary granule component, major basic protein-1 (mMBP-1). The loss of mMBP-1 had no effect on OVA-induced airway histopathologies or inflammatory cell recruitment. Lung function measurements of knockout mice demonstrated a generalized hyporeactivity to methacholine-induced airflow changes (relative to wild type); however, this baseline phenotype was observable only with methacholine; no relative airflow changes were observed in response to another nonspecific stimulus (serotonin). Moreover, OVA sensitization\/aerosol challenge of wild-type and mMBP-1\u2212\/\u2212 mice resulted in identical dose-response changes to either methacholine or serotonin. Thus, the airway hyper-responsiveness in murine models of asthma occurs in the absence of mMBP-1.<\/jats:p>","DOI":"10.4049\/jimmunol.165.10.5509","type":"journal-article","created":{"date-parts":[[2014,4,21]],"date-time":"2014-04-21T23:07:29Z","timestamp":1398121649000},"page":"5509-5517","source":"Crossref","is-referenced-by-count":100,"title":["Eosinophil Major Basic Protein-1 Does Not Contribute to Allergen-Induced Airway Pathologies in Mouse Models of Asthma"],"prefix":"10.1093","volume":"165","author":[{"given":"Karen L","family":"Denzler","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Mayo Clinic Scottsdale, Samuel C. Johnson Medical Research Building , Scottsdale, AZ 85259"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven C","family":"Farmer","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Mayo Clinic Scottsdale, Samuel C. Johnson Medical Research Building , Scottsdale, AZ 85259"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey R","family":"Crosby","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Mayo Clinic Scottsdale, Samuel C. Johnson Medical Research Building , Scottsdale, AZ 85259"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Borchers","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Mayo Clinic Scottsdale, Samuel C. Johnson Medical Research Building , Scottsdale, AZ 85259"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Grzegorz","family":"Cieslewicz","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Mayo Clinic Scottsdale, Samuel C. 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