by Christina Bannert, Bettina Bidmon-Fliegenschnee, Georg Stary, Florian Hotzy, Judith Stift, Samuel Nurko, Zsolt Szépfalusi, Edda Fiebiger, Eleonora Dehlink
The role of the high affinity IgE receptor, FceRI, in IgE-mediated immune responses of the gastrointestinal (GI) mucosa is poorly understood. Currently, a detailed characterization of FceRI expression throughout the human gut is lacking. The aim of this study was to define the expression pattern of FceRI in the GI tract. Methods/Principal Findings
We compared FceRI expression in children with gastritis/esophagitis (n?=?10), celiac disease (n?=?10), inflammatory bowel disease (IBD) (n?=?9), and normal mucosa (n?=?5). The a–subunit of FceRI (FceRIa), detected by immunohistochemistry, was found on cells infiltrating the mucosa of the esophagus, the stomach, and the duodenum, but was rarely detected in more distal sections of the GI tract. Accordingly, quantitative RT-PCR analysis on esophagus, stomach, duodenum, colon, and rectum biopsies revealed that FceRIa and -ß expression levels decreased towards the distal intestine. mRNA transcripts of the common Fc-receptor-? chain were present in the entire GI mucosa. Double-immunofluorescence staining of esophageal specimens confirmed that FceRIa was expressed on intraepithelial mast cells and Langerhans cells. The mRNA expression levels of the a, ß, and ? subunits of FceRI did not correlate with total serum IgE but were associated with mucosal inflammation. Conclusion/Significance
Our data define the upper GI tract as the main site for IgE-mediated immune activation via FceRI. Tissue mRNA levels of FceRIa are regulated by inflammatory conditions rather than serum IgE, indicating that FceRI might also play a role in pathologies other than allergy.