Abstract
IntroductionTGF-β is an important mediator of pulmonary allergic inflammation, and it has been recently reported to be a potential inhibitor of lung tumor progression. The correlation between cancer and allergic inflammatory diseases remains controversial. Thus, the aim of the present study was to evaluate the effects of pulmonary allergic inflammation and in particular the role of TGF-β on cancer progression.MethodsCancer cells were implanted in a BALB/c mice model of allergic airway inflammation, and tumor growth was measured. Apoptosis was evaluated by TUNEL assay, and TGF-β was measured by ELISA. Expression of proliferating cell nuclear antigen, TGF-β, TGF-β receptors I and II, phospho-Smad2 and phospho-Smad4 was evaluated by immunohistochemistry and quantified using digital pathology. The effect of a TGF-β activity inhibitor and recombinant TGF-β on tumor growth was analyzed. The effect of exogenous TGF-β on cell proliferation and apoptosis was evaluated in vitro.ResultsMice with allergic airway inflammation exhibited decreased tumor volumes due to cell proliferation inhibition and increased apoptosis. TGF-β was increased in the sera and tumor tissues of allergic mice. TGF-β activity inhibition increased tumor progression in allergic mice by enhancing proliferation and decreasing apoptosis of tumor cells. The administration of TGF-β resulted in reduced tumor growth.ConclusionThis study is the first to establish an inverse relationship between allergic airway inflammation and tumor progression. This effect appears to be mediated by TGF-β, which is overexpressed in tumor cells during pulmonary allergic inflammation. This study indicates that TGF-β is a potential target for antitumor therapy.Electronic supplementary materialThe online version of this article (doi:10.1007/s00262-015-1722-4) contains supplementary material, which is available to authorized users.
Highlights
transforming growth factor β (TGF-β) is an important mediator of pulmonary allergic inflammation, and it has been recently reported to be a potential inhibitor of lung tumor progression
Allergic airway inflammation inhibits cancer progression in an experimental mice model To evaluate whether the immunologic conditions of allergic inflammation affect tumor progression, we used a mice model of allergic airway inflammation that was previously established by our research group [23, 24]
These two processes have been studied together in a single experimental model, currently, no studies have evaluated the functional effects of pulmonary allergic inflammation, which is characteristic of asthma, on breast cancer progression
Summary
TGF-β is an important mediator of pulmonary allergic inflammation, and it has been recently reported to be a potential inhibitor of lung tumor progression. The aim of the present study was to evaluate the effects of pulmonary allergic inflammation and in particular the role of TGF-β on cancer progression. One of the most important cytokines known to mediate allergic reactions is transforming growth factor β (TGF-β), which is an important fibrogenic factor and immune modulator that may play a relevant role in generating structural airway changes in asthma patients [8,9,10,11]. In vivo and in vitro studies have demonstrated that TGF-β acts as a proinflammatory cytokine, initiating and enhancing inflammation during airway immune responses. This cytokine is involved in airway remodeling, in the development of sub-epithelial fibrosis. A significant increase in TGF-β has been observed in the bronchial lavage of asthma patients, suggesting that the level of this cytokine is directly correlated with the severity of disease [9, 12, 14]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
