Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 116, Issue 2, Pages 536-547Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI26679
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Funding
- NIAID NIH HHS [R01 AI045898, R01 AI45898] Funding Source: Medline
- NIDDK NIH HHS [R24 DK064403] Funding Source: Medline
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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.
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