The function/efficacy of S-IgA in CF is thus difficult to address although Marshall et al. demonstrated that SC ability to neutralize IL-8/CXCL8 is reduced, leading to neutrophilic inflammation [112], and that this reduction is caused by defective glycosylation, essential for SC antimicrobial roles [102] and proper localization of S-IgA at the interface between the lumen and the epithelium [99]. Here, CXCL8 is linked to cystic fibrosis.