Background: COPD is an independent risk factor for lung cancer. Chronic inflammation facilitates tumor development through non immune and immune mechanisms including the perturbation of myelopoiesis resulting in deficiency in Ag-presenting cells and dysfunctional cell-mediated antitumor immunity. We hypothesize that chronic systemic inflammation characteristic of COPD is associated with an expansion of cell populations that suppress antitumor immunity and that these changes are even more evident in COPD with lung cancer (LC). Methods: The percentage of myeloid derived suppressor cells (MDSC) and dendritic cells (DCs) from blood was quantified by flow cytometry in 18 patients with COPD (mean±SD,FEV1=62±23%); 21 smokers with normal lung function (SM) (FEV1= 106±15%pred);26 non-smokers (NSC) (FEV1= 111±14%pred); 19 COPD with LC (COPD LC) (FEV1=71±20%pred) and 8 smokers with LC (SM LC) (FEV1=103±21%pred). Results: COPD patients had an increased number of MDSC (median, range: 79.2, 817 cells x mm 3 ) as compared to NSC (21.1, 338; p=0,02). In addition they showed a reduced percentage of DCs with respect to NSC (0.4, 1%; 0.6; 8%; p=0,02, respectively). To test whether the presence of LC influences these cell populations we compared COPD patients with patients with LC but we did not find any statistically significant result. However, the ratio between MDSC/DC progressively increased in patients with COPD and LC (NSC:0,6; SM:1,2; COPD:2; SM LC: 2,3;COPD LC:3,3). Conclusions: In COPD patients there is an altered pattern of blood MDSC and DCs suggesting a blunted antitumor immunity in this disease as a potential link between inflammation and cancer. These findings are similar to those evident in patients with LC.
Scrimini et al. (Thu,) studied this question.