Mercè Mateu-Jimenez1, Víctor Curull1, Lara Pijuan2, Albert Sánchez-Font1, Hugo Rivera-Ramos3, Alberto Rodríguez-Fuster4, Rafael Aguiló4, Joaquim Gea1, Esther Barreiro5. 1. Pulmonology Department, Lung Cancer and Muscle Research Group, Hospital del Mar Medical Research Institute, Health Park Mar, Health and Experimental Sciences Department, Pompeu Fabra University, Autonomous University of Barcelona, Biomedical Barcelona Research Park, Barcelona, Spain; Center of Biomedical Research Network of Respiratory diseases (CIBERES), Carlos III Health Institute, Barcelona, Spain. 2. Pathology Department, Hospital del Mar Medical Research Institute, Health Park Mar, Barcelona, Spain. 3. Pulmonology Department, Lung Cancer and Muscle Research Group, Hospital del Mar Medical Research Institute, Health Park Mar, Health and Experimental Sciences Department, Pompeu Fabra University, Autonomous University of Barcelona, Biomedical Barcelona Research Park, Barcelona, Spain. 4. Thoracic Surgery Department, Hospital del Mar Medical Research Institute, Health Park Mar, Barcelona, Spain. 5. Pulmonology Department, Lung Cancer and Muscle Research Group, Hospital del Mar Medical Research Institute, Health Park Mar, Health and Experimental Sciences Department, Pompeu Fabra University, Autonomous University of Barcelona, Biomedical Barcelona Research Park, Barcelona, Spain; Center of Biomedical Research Network of Respiratory diseases (CIBERES), Carlos III Health Institute, Barcelona, Spain. Electronic address: ebarreiro@imim.es.
Abstract
INTRODUCTION: Chronic respiratory conditions, especially chronic obstructive pulmonary disease (COPD), and inflammatory events underlie lung cancer (LC). We hypothesized that profiles of T helper 1 and T helper 2 cytokines and type 1 and type 2 macrophages (M1 and M2) are differentially expressed in lung tumors and blood of patients with NSCLC with and without COPD and that the ratio M1/M2 specifically may influence their survival. METHODS: In blood, inflammatory cytokines (determined by enzyme-linked immunosorbent assay) were quantified in 80 patients with LC (60 with LC and COPD [the LC-COPD group] and 20 with LC only [the LC-only group]) and lung specimens (tumor and nontumor) from those undergoing thoracotomy (20 in the LC-COPD group and 20 in the LC-only group). RESULTS: In the LC-COPD group compared with in the LC-only group, systemic levels of tumor necrosis factor-α, interleukin-2 (IL-2), transforming growth factor-β, and IL-10 were increased, whereas vascular endothelial growth factor and IL-4 levels were decreased. In lung tumors, levels of tumor necrosis factor-α, transforming growth factor-β, and IL-10 were higher than in nontumor parenchyma in the LC-COPD group, whereas IL-2 and vascular endothelial growth factor levels were higher in tumors of both the LC-only and LC-COPD groups. Compared with in nontumor lung, M1 macrophage counts were reduced whereas M2 counts were increased in tumors of both patient groups, and the M1/M2 ratio was higher in the LC-COPD group than the LC-only group. M1 and M2 counts did not influence patients' survival. CONCLUSIONS: The relative predominance of T helper 1 cytokines and M1 macrophages in the blood and tumors of patients with underlying COPD imply that a stronger proinflammatory pattern exists in these patients. Inflammation should not be targeted systematically in all patients with LC. Screening for the presence of underlying respiratory diseases and identification of the specific inflammatory pattern should be carried out in patients with LC, at least in early stages of their disease.
INTRODUCTION: Chronic respiratory conditions, especially chronic obstructive pulmonary disease (COPD), and inflammatory events underlie lung cancer (LC). We hypothesized that profiles of T helper 1 and T helper 2 cytokines and type 1 and type 2 macrophages (M1 and M2) are differentially expressed in lung tumors and blood of patients with NSCLC with and without COPD and that the ratio M1/M2 specifically may influence their survival. METHODS: In blood, inflammatory cytokines (determined by enzyme-linked immunosorbent assay) were quantified in 80 patients with LC (60 with LC and COPD [the LC-COPD group] and 20 with LC only [the LC-only group]) and lung specimens (tumor and nontumor) from those undergoing thoracotomy (20 in the LC-COPD group and 20 in the LC-only group). RESULTS: In the LC-COPD group compared with in the LC-only group, systemic levels of tumor necrosis factor-α, interleukin-2 (IL-2), transforming growth factor-β, and IL-10 were increased, whereas vascular endothelial growth factor and IL-4 levels were decreased. In lung tumors, levels of tumor necrosis factor-α, transforming growth factor-β, and IL-10 were higher than in nontumor parenchyma in the LC-COPD group, whereas IL-2 and vascular endothelial growth factor levels were higher in tumors of both the LC-only and LC-COPD groups. Compared with in nontumor lung, M1 macrophage counts were reduced whereas M2 counts were increased in tumors of both patient groups, and the M1/M2 ratio was higher in the LC-COPD group than the LC-only group. M1 and M2 counts did not influence patients' survival. CONCLUSIONS: The relative predominance of T helper 1 cytokines and M1 macrophages in the blood and tumors of patients with underlying COPD imply that a stronger proinflammatory pattern exists in these patients. Inflammation should not be targeted systematically in all patients with LC. Screening for the presence of underlying respiratory diseases and identification of the specific inflammatory pattern should be carried out in patients with LC, at least in early stages of their disease.
Authors: Yingchen Xia; Jianhua Zha; Víctor Curull; Albert Sánchez-Font; Maria Guitart; Alberto Rodríguez-Fuster; Rafael Aguiló; Esther Barreiro Journal: ERJ Open Res Date: 2022-07-18
Authors: Nicola Principe; Joel Kidman; Richard A Lake; Willem Joost Lesterhuis; Anna K Nowak; Alison M McDonnell; Jonathan Chee Journal: Front Oncol Date: 2021-04-27 Impact factor: 6.244