{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T01:06:29Z","timestamp":1791421589477,"version":"4.3.3"},"reference-count":45,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2013,11,4]],"date-time":"2013-11-04T00:00:00Z","timestamp":1383523200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Int Forum Allergy Rhinol"],"published-print":{"date-parts":[[2014,1]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Chronic rhinosinusitis with nasal polyps (CRSwNP) is a disorder characterized by eosinophilic inflammation and local T\u2010helper 2 (Th2) cytokine production. Innate lymphoid cells that elaborate Th2 cytokines have recently been characterized within nasal polyps. These cells can be activated by the epithelial cell\u2010derived cytokine interleukin\u201033 (IL\u201033). The objective of this study is to determine whether 2 molecules associated with tissue damage (high mobility group box\u20101 [HMGB\u20101] and adenosine triphosphate [ATP]) elicit expression of IL\u201033 in sinonasal epithelial cells (SNECs) derived from recalcitrant CRSwNP patients.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Ethmoid tissue was obtained from 8 recalcitrant CRSwNP and 9 control subjects during endoscopic sinus surgery (ESS). Tissue was prepared for immunohistochemistry and for SNEC air\u2010liquid interface culture. After exposure to either HMGB1 or ATP in vitro, SNECs were processed for messenger RNA (mRNA) extraction and immunocytochemistry. IL\u201033 levels were determined by real\u2010time polymerase chain reaction (PCR) and by immunochemical staining with anti\u2010IL\u201033 antibody.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Intranuclear IL\u201033 is normally expressed in basal epithelial cells, but is present in more apical cells and outside the nucleus in CRSwNP. Exposure of SNECs to HMGB\u20101 or ATP resulted in a statistically significant increase in IL\u201033 mRNA expression in SNECs derived from recalcitrant CRSwNP patients. This increase was reflected at the protein level by immunochemical staining of IL\u201033.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Tissue damage is a nonspecific trigger of epithelial IL\u201033 production in treatment\u2010recalcitrant polyps, which may be responsible for perpetuating eosinophilic inflammation in CRSwNP. This common pathway may help explain why multiple environmental and infectious agents have been implicated in CRSwNP exacerbation.<\/jats:p><\/jats:sec>","DOI":"10.1002\/alr.21237","type":"journal-article","created":{"date-parts":[[2013,11,4]],"date-time":"2013-11-04T17:24:38Z","timestamp":1383585878000},"page":"15-21","source":"Crossref","is-referenced-by-count":43,"title":["Damage\u2010associated molecular patterns stimulate interleukin\u201033 expression in nasal polyp epithelial cells"],"prefix":"10.1002","volume":"4","author":[{"given":"Gina","family":"Paris","sequence":"first","affiliation":[{"name":"Department of Otolaryngology\u2013Head and Neck Surgery Johns Hopkins University School of Medicine  Baltimore MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tatyana","family":"Pozharskaya","sequence":"additional","affiliation":[{"name":"Department of Otolaryngology\u2013Head and Neck Surgery Johns Hopkins University School of Medicine  Baltimore 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