Rationale: Chronic obstructive pulmonary disease (COPD) is mainly caused by cigarette smoking, and is characterized by an ongoing inflammatory process and by continuous episodes of infection. Recently, at least two main dendritic cell (DC) subsets have been identified based on origin, phenotype and function. However, little is known of their number and phenotype in COPD patients. Aim: To enumerate peripheral DCs subsets in patients with moderate to severe COPD. Materials and Methods: Venous blood samples were obtained from 15 stable COPD patients (mean FEV1:45 [range:32-63] % of predicted; mean age: 63 [range: 56-68] yrs; 2 current smokers and 8 ex-smokers) and from 15 healthy age-matched non-smoker controls. Phenotypic characterization of type-1 and type-2 myeloid (m) and of plasmacytoid (p) DCs were performed by flow cytometry (DC enumeration kit, Miltenyi Biotec, Germany). Results: Percentages of CD11c+ CD1c+ type-1 mDCs and of CD11c+ CD141+ type-2 mDCs in COPD patients were quite similar to those in healthy controls (mean value±SD: 0.56±0.19 vs 0.72±0.19, and 0.05±0.02 vs 0.04±0.01, respectively, p=ns). In contrast, COPD patients had a reduced percentage of CD123+ CD62L+ pDCs than healthy volunteers (mean value±SD: 0.28±0.20 vs 0.52±0.36, p<0.05), with an higher mDCs:pDCs ratio (2.9±1.8 vs 1.6±0.9). No correlation was found between DCs subsets and airways obstruction. Conclusions: Preliminary data suggest that peripheral pDCs are reduced in moderate to severe COPD patients. While pDCs drive antiviral immune responses, the functional consequences of such a finding in COPD pathogenesis have yet to be determined.
Characterization of peripheral subsets of dendritic cells in COPD patients: preliminary data
VATRELLA, Alessandro;
2008-01-01
Abstract
Rationale: Chronic obstructive pulmonary disease (COPD) is mainly caused by cigarette smoking, and is characterized by an ongoing inflammatory process and by continuous episodes of infection. Recently, at least two main dendritic cell (DC) subsets have been identified based on origin, phenotype and function. However, little is known of their number and phenotype in COPD patients. Aim: To enumerate peripheral DCs subsets in patients with moderate to severe COPD. Materials and Methods: Venous blood samples were obtained from 15 stable COPD patients (mean FEV1:45 [range:32-63] % of predicted; mean age: 63 [range: 56-68] yrs; 2 current smokers and 8 ex-smokers) and from 15 healthy age-matched non-smoker controls. Phenotypic characterization of type-1 and type-2 myeloid (m) and of plasmacytoid (p) DCs were performed by flow cytometry (DC enumeration kit, Miltenyi Biotec, Germany). Results: Percentages of CD11c+ CD1c+ type-1 mDCs and of CD11c+ CD141+ type-2 mDCs in COPD patients were quite similar to those in healthy controls (mean value±SD: 0.56±0.19 vs 0.72±0.19, and 0.05±0.02 vs 0.04±0.01, respectively, p=ns). In contrast, COPD patients had a reduced percentage of CD123+ CD62L+ pDCs than healthy volunteers (mean value±SD: 0.28±0.20 vs 0.52±0.36, p<0.05), with an higher mDCs:pDCs ratio (2.9±1.8 vs 1.6±0.9). No correlation was found between DCs subsets and airways obstruction. Conclusions: Preliminary data suggest that peripheral pDCs are reduced in moderate to severe COPD patients. While pDCs drive antiviral immune responses, the functional consequences of such a finding in COPD pathogenesis have yet to be determined.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
