{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T00:45:36Z","timestamp":1772930736593,"version":"3.50.1"},"reference-count":34,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[1998,6,1]],"date-time":"1998-06-01T00:00:00Z","timestamp":896659200000},"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":[[1998,6,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>A murine model of asthma is described in which we examined the role of intercellular adhesion molecule-1 (ICAM-1) in the pathogenesis of airway reactivity, pulmonary eosinophilia, and inflammation. We sensitized wild-type control [C57BL\/6J, (+\/+)] and ICAM-1 knockout [C57BL\/6J-ICAM-1, (\u2212\/\u2212)] mice to ovalbumin (OVA), and challenged them with OVA delivered by aerosol (OVA-OVA) to induce a phenotype consistent with an asthmatic response. Bronchial responsiveness to methacholine and counts of cell numbers and measurements of eosinophil content and cytokine levels in bronchoalveolar lavage fluid (BALF) were significantly attenuated in ICAM-1\u2212\/\u2212 mice as compared with (+\/+) mice. We also showed that the absence of ICAM-1 had no significant affects on the production of serum IgE antibody, but did have an effect on ex vivo lymphocyte proliferation. Additionally, immunohistochemistry: (1) revealed increased staining for vascular cell adhesion molecule-1 (VCAM-1) after antigen challenge in the ICAM-1\u2212\/\u2212 mice but not in the ICAM-1+\/+ controls; and (2) confirmed the presence of alternatively spliced forms of ICAM-1 in the lungs of ICAM-1\u2212\/\u2212 mice. Thus, despite the availability of alternate adhesion pathways in ICAM-1\u2212\/\u2212 mice, the absence of ICAM-1 prevented eosinophils from entering the airways. In summary, we found that the ICAM-1 knockout mice exhibited a significantly inhibited response to aerosol antigen challenge for most of the parameters examined, and conclude that ICAM-1 is an important ligand mediating T-cell proliferation in response to antigen, eosinophil migration into the airways, and the development of airway hyperreactivity (AHR) in allergen-sensitized and -challenged mice.<\/jats:p>","DOI":"10.1165\/ajrcmb.18.6.3056","type":"journal-article","created":{"date-parts":[[2013,4,3]],"date-time":"2013-04-03T22:14:57Z","timestamp":1365027297000},"page":"777-785","source":"Crossref","is-referenced-by-count":37,"title":["Reduction of Antigen-induced Airway Hyperreactivity and Eosinophilia in ICAM-1-deficient Mice"],"prefix":"10.1093","volume":"18","author":[{"given":"Walter W.","family":"Wolyniec","sequence":"first","affiliation":[{"name":"Department of Immunological Diseases, Research and Development Center, Boehringer Ingelheim Pharmaceuticals Inc., Ridgefield, Connecticut; Pulmonary and Critical Care Divisions, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts; and Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"George T.","family":"De Sanctis","sequence":"additional","affiliation":[{"name":"Department of Immunological Diseases, Research and Development Center, Boehringer Ingelheim Pharmaceuticals Inc., Ridgefield, Connecticut; Pulmonary and Critical Care Divisions, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts; and Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gerald","family":"Nabozny","sequence":"additional","affiliation":[{"name":"Department of Immunological Diseases, Research and Development Center, Boehringer Ingelheim Pharmaceuticals Inc., Ridgefield, Connecticut; Pulmonary and Critical Care Divisions, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts; and Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carol","family":"Torcellini","sequence":"additional","affiliation":[{"name":"Department of Immunological Diseases, Research and Development Center, Boehringer Ingelheim Pharmaceuticals Inc., Ridgefield, Connecticut; Pulmonary and Critical Care Divisions, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts; and Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nancy","family":"Haynes","sequence":"additional","affiliation":[{"name":"Department of Immunological Diseases, Research and Development Center, Boehringer Ingelheim Pharmaceuticals Inc., Ridgefield, Connecticut; Pulmonary and Critical Care Divisions, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts; and Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anthony","family":"Joetham","sequence":"additional","affiliation":[{"name":"Department of Immunological Diseases, Research and Development Center, Boehringer Ingelheim Pharmaceuticals Inc., Ridgefield, Connecticut; Pulmonary and Critical Care Divisions, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts; and Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Erwin W.","family":"Gelfand","sequence":"additional","affiliation":[{"name":"Department of Immunological Diseases, Research and Development Center, Boehringer Ingelheim Pharmaceuticals Inc., Ridgefield, Connecticut; Pulmonary and Critical Care Divisions, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts; and Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeffrey M.","family":"Drazen","sequence":"additional","affiliation":[{"name":"Department of Immunological Diseases, Research and Development Center, Boehringer Ingelheim Pharmaceuticals Inc., Ridgefield, Connecticut; Pulmonary and Critical Care Divisions, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts; and Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas C.","family":"Noonan","sequence":"additional","affiliation":[{"name":"Department of Immunological Diseases, Research and Development Center, Boehringer Ingelheim Pharmaceuticals Inc., Ridgefield, Connecticut; Pulmonary and Critical Care Divisions, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts; and Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[1998,6,1]]},"reference":[{"key":"2026030700183791200_B1","doi-asserted-by":"crossref","first-page":"661","DOI":"10.1016\/0091-6749(91)90160-P","article-title":"Eosinophils, T-lymphocytes, mast cells, neutrophils, and macrophages in bronchial biopsy specimens from atopic subjects with asthma: comparison with biopsy specimens from atopic subjects without asthma and normal control subjects and relationship to bronchial hyperresponsiveness.","volume":"88","author":"Bradley","year":"1991","journal-title":"J. Allergy Clin. Immunol."},{"key":"2026030700183791200_B2","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1084\/jem.183.1.1","article-title":"Sorting out the cytokines of asthma [comment].","volume":"183","author":"Drazen","year":"1996","journal-title":"J. Exp. Med."},{"key":"2026030700183791200_B3"},{"key":"2026030700183791200_B4","first-page":"598","article-title":"Airway hyperresponsiveness, elevation of serum-specific IgE and activation of T cells following allergen exposure in sensitized Brown-Norway rats.","volume":"85","author":"Haczku","year":"1995","journal-title":"Immunology"},{"key":"2026030700183791200_B5","doi-asserted-by":"crossref","first-page":"456","DOI":"10.1126\/science.1967851","article-title":"Intercellular adhesion molecule-1 (ICAM-1) in the pathogenesis of asthma.","volume":"247","author":"Wegner","year":"1990","journal-title":"Science"},{"key":"2026030700183791200_B6"},{"key":"2026030700183791200_B7","doi-asserted-by":"crossref","first-page":"42","DOI":"10.1159\/000232736","article-title":"Induction of adjuvant-independent IgE responses in inbred mice: primary, secondary, and persistent IgE responses to ovalbumin and ovomucoid.","volume":"65","author":"Holt","year":"1981","journal-title":"Int. Arch. Allergy Appl. Immunol."},{"key":"2026030700183791200_B8","doi-asserted-by":"crossref","first-page":"1527","DOI":"10.1084\/jem.182.5.1527","article-title":"Interleukin 12 inhibits antigen-induced airway hyperresponsiveness, inflammation, and Th2 cytokine expression in mice.","volume":"182","author":"Gavett","year":"1995","journal-title":"J. Exp. Med."},{"key":"2026030700183791200_B9","doi-asserted-by":"crossref","first-page":"195","DOI":"10.1084\/jem.183.1.195","article-title":"Interleukin 5 deficiency abolishes eosinophilia, airways hyperreactivity, and lung damage in a mouse asthma model [see comments].","volume":"183","author":"Foster","year":"1996","journal-title":"J. Exp. Med."},{"key":"2026030700183791200_B10","doi-asserted-by":"crossref","first-page":"83","DOI":"10.1159\/000236807","article-title":"Characterization of a murine model of allergic pulmonary inflammation.","volume":"105","author":"Kung","year":"1994","journal-title":"Int. Arch. Allergy Immunol."},{"key":"2026030700183791200_B11","doi-asserted-by":"crossref","first-page":"109","DOI":"10.1084\/jem.183.1.109","article-title":"Interleukin-4, but not interleukin-5 or eosinophils, is required in a murine model of acute airway hyperreactivity [see comments].","volume":"183","author":"Corry","year":"1996","journal-title":"J. Exp. Med."},{"key":"2026030700183791200_B12","first-page":"345","article-title":"Expression and probable roles of cell adhesion molecules in lung inflammation.","volume":"101(Suppl.)","author":"Wegner","year":"1992","journal-title":"Chest"},{"key":"2026030700183791200_B13","first-page":"3","article-title":"Role of eosinophils and cell adhesion molecules in the allergen-induced asthmatic response of rats.","volume":"90","author":"Uyama","year":"1995","journal-title":"Res. Commun. Mol. Pathol. 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Crit. Care Med."},{"key":"2026030700183791200_B18","doi-asserted-by":"crossref","first-page":"243","DOI":"10.1016\/0014-2999(95)00340-Q","article-title":"Role of the VLA-4 integrins in leukocyte recruitment and bronchial hyperresponsiveness in the guinea-pig.","volume":"282","author":"Milne","year":"1995","journal-title":"Eur. J. Pharmacol."},{"key":"2026030700183791200_B19"},{"key":"2026030700183791200_B20","doi-asserted-by":"crossref","first-page":"425","DOI":"10.1038\/346425a0","article-title":"Adhesion receptors of the immune system.","volume":"346","author":"Springer","year":"1990","journal-title":"Nature"},{"key":"2026030700183791200_B21","first-page":"2362","article-title":"Role of the intercellular adhesion molecule-1 (ICAM-1) in endotoxin-induced pneumonia evaluated using ICAM-1 antisense oligonucleotides, anti-ICAM-1 monoclonal antibodies, and ICAM-1 mutant mice.","volume":"97","author":"Kumasaka","year":"1996","journal-title":"J. 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Care Med."}],"container-title":["American Journal of Respiratory Cell and Molecular Biology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/academic.oup.com\/ajrcmb\/article-pdf\/18\/6\/777\/67212486\/ajrcmb_18_6_777.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/academic.oup.com\/ajrcmb\/article-pdf\/18\/6\/777\/67212486\/ajrcmb_18_6_777.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,3,7]],"date-time":"2026-03-07T05:28:07Z","timestamp":1772861287000},"score":1,"resource":{"primary":{"URL":"https:\/\/academic.oup.com\/ajrcmb\/article\/18\/6\/777\/8504473"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1998,6,1]]},"references-count":34,"journal-issue":{"issue":"6","published-online":{"date-parts":[[1998,6,1]]},"published-print":{"date-parts":[[1998,6,1]]}},"URL":"https:\/\/doi.org\/10.1165\/ajrcmb.18.6.3056","relation":{},"ISSN":["1535-4989","1044-1549"],"issn-type":[{"value":"1535-4989","type":"electronic"},{"value":"1044-1549","type":"print"}],"subject":[],"published-other":{"date-parts":[[1998,6]]},"published":{"date-parts":[[1998,6,1]]}}}