| pubmed-article:9144526 | pubmed:abstractText | IL-13, like IL-4, induces up-regulation of vascular cell adhesion molecule-1 (VCAM-1) expression on human endothelial cells in vitro. This may contribute to local accumulation of alpha4beta1+ inflammatory cells, such as eosinophils, macrophages, and T cells. We tested the hypothesis that in human allergic inflammatory reactions in vivo, IL-13 and IL-4 are both involved in VCAM-1/alpha4beta1-dependent recruitment of inflammatory cells. Cryostat cutaneous sections from 13 atopic subjects taken 6, 24, and 48 h after allergen challenge were processed for immunohistochemical staining and in situ hybridization using mAbs and 35S-labeled riboprobes for IL-4 and IL-13. When compared with diluent sites, allergen provoked significant increases in the numbers of cells that were mRNA+ and protein-positive for both IL-13 and IL-4 that were clearly demonstrable at 6 h, peaked at 24 h, and declined by 48 h. Double immunohistochemical staining/in situ hybridization showed that the majority (>60%) of IL-13 mRNA+ signals were colocalized to CD3+ T cells. The numbers of mRNA+ and protein-positive cells for IL-13 significantly correlated with VCAM-1 immunoreactivity on endothelial cells and with total numbers of infiltrating EG2+ eosinophils, CD45RO+ T cells, and CD68+ macrophages, but not elastase-positive neutrophils, at the 6- and 24-h time points. At 6 h, an association was also observed between the numbers of IL-4 mRNA+ or protein product-positive cells and VCAM-1 expression, although this was not statistically significant. These findings suggest that IL-13 may play an important role in recruitment of inflammatory cells to the site of cutaneous allergic inflammatory reaction through VCAM-1/alpha4beta1-dependent mechanisms. | lld:pubmed |
