Eosinophil infiltration into human skin is antigen-dependent in the late-phase reaction

Abstract

Eosinophils play a critical role in late-phase reaction allergic inflammatory responses, although the factors responsible for selective tissue eosinophilia are currently ill-defined. To determine whether recruitment of eosinophils is allergen-specific, or a feature of inflammation in allergic individuals, we have examined cutaneous cell infiltrates and endothelial cell adhesion molecule expression in atopic subjects 6 h (n = 8) and 24 h (n = 7) following ultraviolet-B (UVB) irradiation, or intradermal injection of late-phase reaction allergens or diluent control, using standard immunohistochemical techniques. The numbers of eosinophils were increased significantly, when compared to controls, at both 6 h (P < 0.01) and 24 h (P < 0.05), following intradermal allergen challenge, whereas no significant increase in eosinophils was observed following UVB irradiation. UVB and allergen both induced significant increases in neutrophils, monocytes and T cells at 24 h compared to control sites. An increased expression of endothelial cell adhesion molecules, E-selectin and intercellular adhesion molecule-1 (ICAM-1), was observed in both models of inflammation. Vascular cell adhesion molecule-1 (VCAM-1) was induced weakly on some biopsies following allergen, and not at all following UVB. These data indicate that eosinophil infiltration in susceptible individuals is a specific property of allergen. Although this study would support the postulated role of VCAM-1 in selective eosinophil recruitment, given its variable and weak expression, additional factors are likely to be involved.

What Can Microdialysis Tell Us About the Temporal and Spatial Generation of Cytokines in Allergen-Induced Responses in Human Skin In Vivo?

“…At the site of allergen injection, biopsies taken at 6 hours showed marked increases in the adhesion molecules E-selectin, ICAM-1, and VCAM-1. Also, there was a 65-fold increase in neutrophils and a 4-fold increase in eosinophils, consistent with previous studies (Barata et al, 1998;Litchfield et al, 1996). However, at the site 1 cm away from allergen injection, there was little staining for adhesion molecules and no inflammatory cell accumulation.…”

Cetirizine inhibits skin reactions but not mediator release in immediate and developing late‐phase allergic cutaneous reactions. A double‐blind, placebo‐controlled study

“…Increase of ECP was evident from 3 h and onwards, and this response was not inhibited by cetirizine. Histological studies have demonstrated an influx of eosinophils into the dermis at 3 h [26] and no effect of cetirizine on eosinophil influx at later time points [13,14,16]. No significant release of MPO was evident, and the eosinophil chemoattractant LTB 4 did not increase significantly over 7 h. The latter finding is in agreement with findings by Kuhns and coworkers [27].…”