RT Journal Article
SR Electronic
T1 Myeloid derived suppressor cells in the crosstalk between COPD and lung cancer
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP p3851
VO 38
IS Suppl 55
A1 Simonetta Baraldo
A1 Laura Pinton
A1 Andrea Ballarin
A1 Susanna Mandruzzato
A1 Erica Bazzan
A1 Erika Falisi
A1 Graziella Turato
A1 Kim Lokar-Oliani
A1 Manuel Cosio
A1 Paola Zanovello
A1 Marina Saetta
YR 2011
UL http://erj.ersjournals.com/content/38/Suppl_55/p3851.abstract
AB COPD is associated to increased lung cancer risk, even independently from cigarette smoke. The chronic inflammation present in COPD patients may represent an important link with lung cancer, but the relationship has yet to be elucidated. Of note tumors, to promote their own survival, may influence the immune response by inducing a subset of myeloid cells with immunosuppressor properties (MDSC). We evaluated the induction of MDSC in patients with COPD, with or without lung cancer, by measuring the α chain of IL-4 receptor (IL4Rα) which has been proposed as a marker for these cells. IL4Rα was quantified by flow cytometry in peripheral blood from 19 smokers with COPD and no cancer (FEV1=56±6%pred), 6 smokers with COPD and lung cancer (FEV1=67±9%pred) and 11 controls with normal lung function and no cancer (5 smoking, 6 non-smoking; FEV1=106±6%pred).IL4Rα expression was increased in monocytes from smokers with COPD and concomitant lung cancer (23;17-37%) but also in COPD subjects without cancer (median;range: 12;5-25%) compared to smoking and non-smoking controls (10;3-15% and 9;7-11%. all p<0.05). A similar IL4Rα upregulation was also observed in granulocytes. Of note, in all patients considered together, IL4Rα expression was related to the degree of airway obstruction (p=0.003,r=-0.50).In conclusion, our study shows that IL4Rα expression is upregulated in monocytes and granulocytes from smokers with COPD and lung cancer, but interestingly even in COPD patients without cancer. Evaluation of the alleged suppressive activity of these cells could improve our understanding of the immune response in COPD and potentially identify inflammatory alterations that might increase the risk of developing lung cancer.