Recent findings of elevated plasma fibronectin (FN) levels in infants with atopic diseases also led to the observation that FN can increase TSLP expression in bronchial epithelium tissue models. The discovery of FN as a potential contributor to epithelial inflammation establishes FN interception as a potential new route for inhibiting type 2 inflammation. FN displays large positively charged patches on its surface, suggesting interaction potential with negatively charged molecules, such as sulfated polyglycerols (PG) and natural polyanions like heparin and the structurally related heparan sulfate. This interaction potential also applies to TSLP, since its binding with TSLPR relies upon electrostatic interaction with negative patches on TSLPR. The significance of these positive charges for the function of both proteins led us to hypothesize that highly charged molecules may interfere with the binding mechanisms that enable these proteins' roles in the inflammatory cascade.