The potential role of interleukin-13 in eosinophilic inflammation in nasal mucosa.

Abstract

Recent studies have revealed that interleukin (IL)-13, as well as IL-4, causes de novo surface expression of vascular cell adhesion molecule-1 (VCAM-1) on endothelial cells of the umbilical vein and accelerates selective eosinophil migration. However, its role in allergic rhinitis remains to be clarified. Of particular interest is whether IL-13 upregulates VCAM-1 expression in human mucosal microvascular endothelial cells (HMMECs), to which eosinophils adhere in nasal mucosa. To understand the potential role of IL-13 in eosinophilic inflammation in nasal mucosa, we examined the effects of IL-13 on the adhesiveness between HMMECs and eosinophils. IL-13 increased VCAM-1 expression in HMMECs, the adhesiveness of endothelial cells to eosinophils, and the transendothelial migration. On the other hand, IL-13 decreased the adhesiveness of eosinophils to HMMECs, and, as a result, accelerated eosinophil infiltration. Those effects are more potent than was those of IL-4. In addition, we also report that the amount of IL-13 in nasal mucosa was higher than that of IL-4. These results strongly indicate that IL-13, as well as IL-4, may be important in eosinophilic inflammation in the nasal mucosa.