{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T21:51:15Z","timestamp":1791669075064,"version":"4.3.4"},"reference-count":56,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2007,11,1]],"date-time":"2007-11-01T00:00:00Z","timestamp":1193875200000},"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":[[2007,11,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Rationale<\/jats:title>\n                    <jats:p>Asthma is characterized by increases in airway resistance, pulmonary remodeling, and lung inflammation. The cytokine transforming growth factor (TGF)-\u03b2 has been shown to have a central role in asthma pathogenesis and in mouse models of allergic airway disease.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To determine the contribution of TGF-\u03b2 to airway hyperresponsiveness (AHR), we examined the time course, source, and isoform specificity of TGF-\u03b2 production in an in vivo mouse asthma model. To then elucidate the function of TGF-\u03b2 in AHR, inflammation, and pulmonary fibrosis, we examined the effects of blocking TGF-\u03b2 signaling with neutralizing antibody.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Mice were sensitized and challenged with ovalbumin (OVA) to establish allergic airway disease. TGF-\u03b2 activity was neutralized by intranasal administration of monoclonal antibody.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>TGF-\u03b21 protein levels were increased in OVA-challenged lungs versus naive controls, and airway epithelial cells were shown to be a likely source of TGF-\u03b21. In addition, TGF-\u03b21 levels were elevated in OVA-exposed IL-5\u2013null mice, which fail to recruit eosinophils into the airways. Neutralization of TGF-\u03b21 with specific antibody had no significant effect on airway inflammation and eosinophilia, although anti\u2013TGF-\u03b21 antibody enhanced OVA-induced AHR and suppressed pulmonary fibrosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These data show that TGF-\u03b21 is the main TGF-\u03b2 isoform produced after OVA challenge, with a likely cellular source being the airway epithelium. The effects of blocking TGF-\u03b21 signaling had differential effects on AHR, fibrosis, and inflammation. While TGF-\u03b2 neutralization may be beneficial to abrogating airway remodeling, it may be detrimental to lung function by increasing AHR.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.200702-334oc","type":"journal-article","created":{"date-parts":[[2007,8,29]],"date-time":"2007-08-29T21:39:19Z","timestamp":1188423559000},"page":"974-982","source":"Crossref","is-referenced-by-count":92,"title":["Transforming Growth Factor-\u03b21 Suppresses Airway Hyperresponsiveness in Allergic Airway Disease"],"prefix":"10.1093","volume":"176","author":[{"given":"John F.","family":"Alcorn","sequence":"first","affiliation":[{"name":"Department of Pathology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa M.","family":"Rinaldi","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Vermont, Burlington, Vermont"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth F.","family":"Jaffe","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Vermont, Burlington, Vermont"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mirjam","family":"van Loon","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Vermont, Burlington, Vermont"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jason H. 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