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

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Abstract
Background 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. Methods 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. Results 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. Conclusions These results strongly indicate that IL‐13. as well as IL‐4, may be important in eosinophilic inflammation in the nasal mucosa.

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