Objectives:: The aim was to investigate the expression of cytokines, adhesion molecules, and activation and proliferation markers in duodenal biopsies from children with delayed‐type food allergy (FA).
Methods:: Seven children with untreated FA (uFA), seven children with treated FA (tFA) to cow milk and/or cereals, and five normal controls furnished duodenal biopsy specimens. Additionally, five pediatric patients with celiac disease were included, serving exclusively as positive controls for in situ hybridization. Interferon‐γ (IFN‐γ), interleukin‐4 (IL‐4), adhesion molecules, and activation markers were detected by immunohistochemistry, and expression of IFN‐γ and IL‐4 messenger RNA was revealed by in situ hybridization.
Results:: uFA patients had a higher density of IFN‐γ positive cells in the lamina propria than did tFA patients and controls (P = 0.053 and P = 0.018). Moreover, the uFA patients exhibited a higher proportion of crypt cells in mitosis than did tFA patients (P = 0.026), and stronger staining of HLA‐DR in the crypts and increased density of γδ‐T cell receptor‐positive intraepithelial lymphocytes than did controls (P = 0.048 and P = 0.010). The densities of α4β7 positive cells in the lamina propria tended to be higher in controls than in uFA or tFA patients (P = 0.106, P = 0.073). Expression of IL‐4 mRNA was significantly higher in celiac patients than in the other study groups (uFA P = 0.006, tFA P = 0.010; controls P = 0.029), and celiac patients showed higher expression of IFN‐γ mRNA than did tFA patients or controls (P = 0.017 and P = 0.016).
Conclusions:: As expected, Th1 dominance was present in the lamina propria of children with delayed‐type FA. It may cause activation of epithelial cells and increase their turnover.
*Hospital for Children and Adolescents, University of Helsinki, Finland; †Ist Department of Pediatrics, Budapest, Hungary; ‡Department of Pediatrics, University of Oulu, Finland
Received July 11, 2002; accepted February 18, 2003.
Corresponding author: Address correspondence to Erkki Savilahti, Hospital for Children and Adolescents, University of Helsinki, Stenbäckinkatu 11, 00029 HUCH, Finland (E‐mail: email@example.com).
G.V. and M.W‐O. contributed equally to this work.
Sources of support: The Sigrid Juselius Foundation, the Foundation of the Friends of the University Children's Hospitals in Finland, the Finnish Medical Association, Finland, the Hungarian National Scientific Research Foundation (OTKA‐T31791), and the Hungarian Medical Scientific Council (ETT‐297/2000). Monoclonal antibody ACT‐1 (anti‐α4β7) was a gift from Leukosite Inc., Cambridge, MA.