AbMole BioScience kinase inhibitors Moreover, one-quarter of patients fail to recover their previous baseline lung function despite therapy, likely because current management is suboptimal. Biomarkers reflective of disease activity in pulmonary exacerbations have the potential to improve patient care. Systemic biomarkers monitoring inflammation are ideal because they could reflect the status of disease activity and severity throughout the entire lung, as opposed to one region as in the case of sputum. Although blood-based biomarkers have been widely studied in CF pulmonary exacerbations, only CRP consistently correlated with disease activity, with increases from stable to exacerbation state and decreases in response to therapy. However, no systemic biomarker, including CRP, has been validated in a clinical trial supporting its clinical usefulness beyond routine clinical assessment. Thus, further research to find out more robust and sensitive biomarkers reflecting the lung disease activity and severity is needed. In this study, we began to approach the systemic biomarker field by a genome-wide evaluation of gene expression in blood neutrophils, the principal immune cell involved in the CF lung inflammation. Our approach was to reduce the dimensions of data in order to focus on a very small but significant number of genes with a limited set of patient samples. This was done by employing differential expression analysis and subsequently verified by PCA. Data presented in this paper show that in blood neutrophils obtained from CF patients there is an overall genic down-regulation compared with healthy subjects, including genes encoding for proteins involved in apoptosis, cell adhesion, inflammatory and immune response. Antibiotic therapy treatment for 10 days reversed this figure to genic up-regulation. These results suggest that blood neutrophils have a defect in apoptosis and activation, a condition brought to “healthy” status by antibiotic therapy. Previously, Adib-Conquy and colleagues published microarray analysis of 1050 genes in blood neutrophils collected from CF patients devoid of bacterial colonization and compared them with healthy subjects. Their list of upregulated and downregulated genes does not include genes found in the present study. This discrepancy might be ascribed to various differences between the two studies: just one of their five patients was F508del/F508del, the mean age was of 10.7 years, the mean FEV1 was 55% of predicted, all parameters which differ substantially from ours. Finally, our patients were all colonized by P. aeruginosa and other bacterial species.