{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,2,21]],"date-time":"2025-02-21T08:15:47Z","timestamp":1740125747918,"version":"3.37.3"},"reference-count":39,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2017,11,16]],"date-time":"2017-11-16T00:00:00Z","timestamp":1510790400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"NIAID NIH","award":["T32AI007635"],"award-info":[{"award-number":["T32AI007635"]}]},{"name":"University of Wisconsin Carbone Cancer Center Support","award":["P30 CA014520"],"award-info":[{"award-number":["P30 CA014520"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunology"],"published-print":{"date-parts":[[2018,4]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Pulmonary challenge with the ubiquitous fungus <jats:italic>Cryptococcus neoformans<\/jats:italic> results in allergic airway inflammation (<jats:styled-content style=\"fixed-case\">AAI<\/jats:styled-content>) characterized by robust recruitment of eosinophils and T cells producing type 2 cytokines to the lungs. Previous studies have demonstrated a critical role for Nuclear Factor Kappa B (<jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010<jats:italic>\u03ba<\/jats:italic>B) activation within lung epithelial cells (<jats:styled-content style=\"fixed-case\">LEC<\/jats:styled-content>s) in driving <jats:styled-content style=\"fixed-case\">AAI<\/jats:styled-content> in response to protein allergens, yet the role of <jats:styled-content style=\"fixed-case\">LEC<\/jats:styled-content>\u2010intrinsic <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010<jats:italic>\u03ba<\/jats:italic>B in promoting <jats:styled-content style=\"fixed-case\">AAI<\/jats:styled-content> following exposure to <jats:italic>C. neoformans<\/jats:italic> is poorly understood. To investigate the role of <jats:styled-content style=\"fixed-case\">LEC<\/jats:styled-content>\u2010intrinsic <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010<jats:italic>\u03ba<\/jats:italic>B in promoting <jats:styled-content style=\"fixed-case\">AAI<\/jats:styled-content> following <jats:italic>C. neoformans<\/jats:italic> challenge, we used <jats:styled-content style=\"fixed-case\">IKK<\/jats:styled-content><jats:sup>\u2206<\/jats:sup><jats:styled-content style=\"fixed-case\"><jats:sup>LEC<\/jats:sup><\/jats:styled-content> mice, which lack canonical <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010<jats:italic>\u03ba<\/jats:italic>B activation specifically within <jats:styled-content style=\"fixed-case\">LEC<\/jats:styled-content>s. <jats:styled-content style=\"fixed-case\">IKK<\/jats:styled-content><jats:sup>\u2206<\/jats:sup><jats:styled-content style=\"fixed-case\"><jats:sup>LEC<\/jats:sup><\/jats:styled-content> and littermate control mice were intranasally challenged with 10<jats:sup>6<\/jats:sup> <jats:styled-content style=\"fixed-case\">CFU<\/jats:styled-content> of <jats:italic>C. neoformans<\/jats:italic> strain 52D, and lung tissues were collected at 7, 14 and 21 days post infection to assess the development of <jats:styled-content style=\"fixed-case\">AAI<\/jats:styled-content>. Notably, the absence of epithelial <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010<jats:italic>\u03ba<\/jats:italic>B signalling did not affect the magnitude or kinetics of lung eosinophilia when compared with the response in wild\u2010type control mice. The total numbers of lung T cells producing the type 2 cytokines interleukin\u20105 and interleukin\u201013 were also unchanged in <jats:styled-content style=\"fixed-case\">IKK<\/jats:styled-content><jats:sup>\u2206<\/jats:sup><jats:styled-content style=\"fixed-case\"><jats:sup>LEC<\/jats:sup><\/jats:styled-content> mice. Furthermore, <jats:styled-content style=\"fixed-case\">IKK<\/jats:styled-content><jats:sup>\u2206<\/jats:sup><jats:styled-content style=\"fixed-case\"><jats:sup>LEC<\/jats:sup><\/jats:styled-content> mice showed no defect in the recruitment of protective interferon\u2010<jats:italic>\u03b3<\/jats:italic>\u2010producing <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4 T cells to the lungs, fungal clearance, or host survival compared with control mice. Immunofluorescence imaging surprisingly revealed no evidence of nuclear localization of <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010<jats:italic>\u03ba<\/jats:italic>B in <jats:styled-content style=\"fixed-case\">LEC<\/jats:styled-content>s in response to <jats:italic>C. neoformans<\/jats:italic> challenge, indicating that <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010<jats:italic>\u03ba<\/jats:italic>B is not activated within these cells. Taken together, these data strongly suggest that <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010<jats:italic>\u03ba<\/jats:italic>B signalling within <jats:styled-content style=\"fixed-case\">LEC<\/jats:styled-content>s does not promote <jats:styled-content style=\"fixed-case\">AAI<\/jats:styled-content> observed in response to <jats:italic>C. neoformans<\/jats:italic>.<\/jats:p>","DOI":"10.1111\/imm.12853","type":"journal-article","created":{"date-parts":[[2017,10,21]],"date-time":"2017-10-21T00:26:39Z","timestamp":1508545599000},"page":"513-522","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Inhaled <i>Cryptococcus neoformans<\/i> elicits allergic airway inflammation independent of Nuclear Factor Kappa B signalling in lung epithelial cells"],"prefix":"10.1111","volume":"153","author":[{"given":"Andrew J.","family":"McDermott","sequence":"first","affiliation":[{"name":"Department of Pediatrics University of Wisconsin School of Medicine and Public Health Madison WI USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tyler A.","family":"Tumey","sequence":"additional","affiliation":[{"name":"Department of Pediatrics University of Wisconsin School of Medicine and Public Health Madison WI USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mingwei","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Biomolecular Chemistry School of Medicine and Public Health University of Wisconsin\u2010Madison Madison WI USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christina M.","family":"Hull","sequence":"additional","affiliation":[{"name":"Department of Biomolecular Chemistry School of Medicine and Public Health University of Wisconsin\u2010Madison Madison WI USA"},{"name":"Department of Medical Microbiology and Immunology University of Wisconsin School of Medicine and Public Health Madison WI 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