Allergic inflammation does not impact chemical-induced carcinogenesis in the lungs of mice

dc.contributor.authorDoris, Konstantinosen
dc.contributor.authorKarabela, Sophia Pen
dc.contributor.authorKairi, Chrysoulaen
dc.contributor.authorSimoes, Davina CMen
dc.contributor.authorRoussos, Charisen
dc.contributor.authorZakynthinos, Spyros Gen
dc.contributor.authorKalomenidis, Ioannisen
dc.contributor.authorBlackwell, Timothy Sen
dc.contributor.authorStathopoulos, Georgios Ten
dc.contributor.otherDoris, Κωνσταντίνοςgr
dc.contributor.otherΚαράμπελα, Σοφία Πgr
dc.contributor.otherΚαΐρη, Χρυσούλαgr
dc.contributor.otherSimoes, Davina CMgr
dc.contributor.otherΡούσσος, Χάρηςgr
dc.contributor.otherΖακυνθινός, Σπύρος Γgr
dc.contributor.otherΚαλομενίδης, Ιωάννηςgr
dc.contributor.otherBlackwell, Timothy Sen
dc.contributor.otherΣταθόπουλος, Γεώργιος Τen
dc.date.accessioned2011-12-02T08:41:46Zen
dc.date.available2011-12-02T08:41:46Zen
dc.date.copyright2010-08-26en
dc.date.issued2011-12-02en
dc.description.abstractAlthough the relationship between allergic inflammation and lung carcinogenesis is not clearly defined, several reports suggest an increased incidence of lung cancer in patients with asthma. We aimed at determining the functional impact of allergic inflammation on chemical carcinogenesis in the lungs of mice. Methods Balb/c mice received single-dose urethane (1 g/kg at day 0) and two-stage ovalbumin during tumor initiation (sensitization: days -14 and 0; challenge: daily at days 6-12), tumor progression (sensitization: days 70 and 84; challenge: daily at days 90-96), or chronically (sensitization: days -14 and 0; challenge: daily at days 6-12 and thrice weekly thereafter). In addition, interleukin (IL)-5 deficient and wild-type C57BL/6 mice received ten weekly urethane injections. All mice were sacrificed after four months. Primary end-points were number, size, and histology of lung tumors. Secondary end-points were inflammatory cells and mediators in the airspace compartment. Results Ovalbumin provoked acute allergic inflammation and chronic remodeling of murine airways, evident by airspace eosinophilia, IL-5 up-regulation, and airspace enlargement. Urethane resulted in formation of atypical alveolar hyperplasias, adenomas, and adenocarcinomas in mouse lungs. Ovalbumin-induced allergic inflammation during tumor initiation, progression, or continuously did not impact the number, size, or histologic distribution of urethane-induced pulmonary neoplastic lesions. In addition, genetic deficiency in IL-5 had no effect on urethane-induced lung tumorigenesis. Conclusions Allergic inflammation does not impact chemical-induced carcinogenesis of the airways. These findings suggest that not all types of airway inflammation influence lung carcinogenesis and cast doubt on the idea of a mechanistic link between asthma and lung cancer.en
dc.description.translatedabstract-en
dc.identifier.urihttp://hdl.handle.net/10889/4832en
dc.language.isoenen
dc.relation.urihttp://dx.doi.org/10.1186/1465-9921-11-118en
dc.sourceRespiratory Research, 11gr
dc.subjectAllergic inflammationgr
dc.subjectLung carcinogenesisgr
dc.subject.alternativeΑλλεργική φλεγμονήen
dc.subject.alternativeΠνευμονική καρκινογένεσηen
dc.titleAllergic inflammation does not impact chemical-induced carcinogenesis in the lungs of miceen
dc.typeJournal (paper)en
dcterms.extent118en

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