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

Doris, Konstantinos

Stathopoulos, Georgios T

Kairi, Chrysoula

Simoes, Davina CM

Blackwell, Timothy S

Kalomenidis, Ioannis

Zakynthinos, Spyros G

Roussos, Charis

Karabela, Sophia P

Καλομενίδης, Ιωάννης

Καράμπελα, Σοφία Π

Simoes, Davina CM

Blackwell, Timothy S

Ρούσσος, Χάρης

Ζακυνθινός, Σπύρος Γ

Doris, Κωνσταντίνος

Σταθόπουλος, Γεώργιος Τ

Καΐρη, Χρυσούλα

Although 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.

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Journal (paper)

Allergic inflammation

Αλλεργική φλεγμονή

Lung carcinogenesis

Πνευμονική καρκινογένεση

Πανεπιστήμιο Πατρών

Νημερτής

http://dx.doi.org/10.1186/1465-9921-11-118

Respiratory Research, 11

Αγγλική γλώσσα

2010-08-26

2011-12-02

2011-12-02T08:41:46Z

http://hdl.handle.net/10889/4832

Respiratory Research, 11