{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T18:31:43Z","timestamp":1790015503147,"version":"4.0.1"},"reference-count":36,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2017,12,1]],"date-time":"2017-12-01T00:00:00Z","timestamp":1512086400000},"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":[[2017,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>IgE contributes to disease exacerbations but not to baseline airway hyperresponsiveness (AHR) in human asthma. In rodent allergic airway disease (AAD), mast cell and IgE dependence for the induction of AHR has only been observed when mice are immunized with a relatively weak allergen without adjuvant. To evaluate the role of IgE in murine AAD that is induced by a potent allergen, we inoculated BALB\/c and FVB\/N background wild-type and IgE- or Fc\u03b5RI\u03b1-deficient mice intratracheally with large or limiting doses of house dust mite extract (HDM) and evaluated AHR, pulmonary eosinophilia, goblet cell metaplasia, serum IgE, and lung mastocytosis. We found that neither IgE nor Fc\u03b5RI\u03b1 contributed to AAD, even in mice inoculated with the lowest dose of HDM, which readily induced detectable disease, but did not increase serum IgE or pulmonary mast cell levels. In contrast, high doses of HDM strikingly increased serum IgE and pulmonary mast cells, although both AHR and airway mast cell degranulation were equally elevated in wild-type and IgE-deficient mice. Surprisingly, allergen challenge of mice with severe AAD and pulmonary mastocytosis failed to acutely increase airway resistance, lung Newtonian resistance, or hysteresis. Overall, this study shows that, although mice may not reliably model acute asthma exacerbations, mechanisms that are IgE and Fc\u03b5RI\u03b1 independent are responsible for AHR and airway inflammation when low doses of a potent allergen are inhaled repetitively.<\/jats:p>","DOI":"10.1165\/rcmb.2016-0356oc","type":"journal-article","created":{"date-parts":[[2017,7,12]],"date-time":"2017-07-12T12:34:43Z","timestamp":1499862883000},"page":"674-682","source":"Crossref","is-referenced-by-count":36,"title":["House Dust Mite\u2013Induced Allergic Airway Disease Is Independent of IgE and Fc\u03b5RI\u03b1"],"prefix":"10.1093","volume":"57","author":[{"given":"Christopher G.","family":"McKnight","sequence":"first","affiliation":[{"name":"Department of Immunology, Allergy and Rheumatology, University of Cincinnati, Cincinnati, Ohio"},{"name":"Medical Service, Cincinnati Veterans Affairs Medical Center, Cincinnati, Ohio"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joseph A.","family":"Jude","sequence":"additional","affiliation":[{"name":"Rutgers Institute for Translational Medicine and Science, New Brunswick, New Jersey"},{"name":"Child Health Institute of New Jersey, Rutgers, State University of New Jersey, New Brunswick, New Jersey"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhenqi","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of Immunology, Allergy and Rheumatology, University of Cincinnati, Cincinnati, Ohio"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr.","given":"Reynold A.","family":"Panettieri","sequence":"additional","affiliation":[{"name":"Child Health Institute of New Jersey, Rutgers, State University of New Jersey, New Brunswick, New Jersey"},{"name":"Rutgers Robert Wood Johnson Medical School, Medicine, Piscataway, New Jersey; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fred 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