Recently, a multicenter cross-sectional study has found significant negative correlations between FEV 1 % predicted and spontaneously expectorated sputum inflammatory markers including free elastase, IL-8, neutrophil counts, and percent neutrophils [32] . In this study we provide evidence, for the first time, of the presence of MPs in sputa obtained from CF patients. The membrane composition of MPs reflects the plasma membrane of the original cell at the precise moment of MPs production and thus allows the characterization of the cellular source [33] using antibodies directed against these specific epitopes. Our data strongly support the notion that MPs are derived from granulocytes, while the presence of MPs derived from monocyte-macrophages is negligible. Although there are several potential sources of sputum MPs, including erythrocytes, platelets, and epithelial cells, our data suggest that granulocytes are the predominant source of MPs in CF. Our findings are consistent with massive influx of neutrophils into CF airways and their accumulation on the surface of the airway epithelium [34] . In this environment, neutrophils are activated by bacterial products, pro-inflammatory cytokines, and chemokines. Neutrophils undergo apoptosis, as normally happens in acute inflammation, but also post-apoptotic necrosis, releasing toxic enzymes and oxygen radicals. MPs in CF sputa likely reflect both activation and apoptosis of neutrophils. In order to evaluate the effect of bacterial infection on MPs production, it would be interesting to compare subgroups based on the presence or absence of infection with Pseudomonas aeruginosa or other bacterial strains, therefore further studies with larger number of patients are needed. PCD patients were selected as controls because healthy donors do not produce spontaneous sputum; moreover, PCD patients have similar respiratory infections to CF patients. In PCD, neutrophilic lung inflammation, incidence of lung infection, offending organisms, development of bronchiectasis and longitudinal declines in lung function are similar to CF but appear to be delayed, and serious lung disease tends to develop later in life [35] [36] [37] . This could be the reason for a significantly less presence of granulocytederived MPs in PCD when compared with CF patients.