Though correction for multiple comparisons was not performed in our study, confirmatory studies in the lower airways as well as in vitro studies using murine and human epithelial monolayers that indicate IP-10 is robustly expressed in response to bacterial infection indicate IP-10 is elevated in CF APE and may also contribute to the pathobiology of CF pulmonary exacerbations. This evidence concerns the gene CXCL10 and bacterial infectious disease.