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

Allergy. 1998 Jul;53(7):690-7. doi: 10.1111/j.1398-9995.1998.tb03955.x.

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.

Publication types

  • Comparative Study

MeSH terms

  • Adolescent
  • Adult
  • Cell Adhesion / drug effects
  • Cell Adhesion / immunology
  • Cell Movement / drug effects
  • Cells, Cultured
  • Endothelium, Vascular / immunology
  • Eosinophils / drug effects*
  • Eosinophils / immunology
  • Humans
  • Interleukin-13 / immunology
  • Interleukin-13 / pharmacology*
  • Interleukin-4 / immunology
  • Interleukin-4 / pharmacology
  • Nasal Mucosa / drug effects*
  • Nasal Mucosa / immunology
  • Time Factors
  • Vascular Cell Adhesion Molecule-1 / metabolism*

Substances

  • Interleukin-13
  • Vascular Cell Adhesion Molecule-1
  • Interleukin-4