Year: 2006
Type: article
Study design: Observational Study
Abstract: Eosinophilic esophagitis (EE) is an emerging disorder with a poorly understood pathogenesis. In order to define disease mechanisms, we took an empirical approach analyzing esophageal tissue by a genome-wide microarray expression analysis. EE patients had a striking transcript signature involving 1% of the human genome that was remarkably conserved across sex, age, and allergic status and was distinct from that associated with non-EE chronic esophagitis. Notably, the gene encoding the eosinophil-specific chemoattractant eotaxin-3 (also known as CCL26) was the most highly induced gene in EE patients compared with its expression level in healthy individuals. Esophageal eotaxin-3 mRNA and protein levels strongly correlated with tissue eosinophilia and mastocytosis. Furthermore, a single-nucleotide polymorphism in the human eotaxin-3 gene was associated with disease susceptibility. Finally, mice deficient in the eotaxin receptor (also known as CCR3) were protected from experimental EE. These results implicate eotaxin-3 as a critical effector molecule for EE and provide insight into disease pathogenesis.
DOI: 10.1172/jci26679
Authors: C. Blanchard, Ning Wang, Keith F Stringer, Anil Mishra, Patricia C Fulkerson, J Pablo Abonia, Sean C Jameson, Cassie Kirby, Michael R Konikoff, Margaret H Collins, Mitchell B Cohen, Rachel Akers, Simon P Hogan, Amal H Assa'ad, Philip E Putnam, Bruce J Aronow, Marc E Rothenberg
Language: English
Topic: Eosinophilic Esophagitis
Subfield: Gastroenterology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W2144846148