In addition to binding with FN, dPGS is likely to interact with other cytokines that induce TSLP release, due to these cytokines' positive surface charge, especially at high concentrations like those we investigated. A broad range of targets has previously been described for polyanions like dPGS and heparins. The previously observed reduction in neutrophil extravasation in the presence of dPGS, primarily attributed to L-and P-selectin inhibition, may also result partially from FN inhibition, given FN's role as an adhesion molecule in immune cell migration. Inhibition of inflammation by FN signal disruption has been observed in murine models of vascular inflammation. Finally, FN is also known to regulate the binding of IL-7 to the cell surface by different stretching of the proteoglycan, an effect that might also be altered by dPGS binding.