RGD Reference Report - Treatment with topical steroids downregulates IL-5, eotaxin-1/CCL11, and eotaxin-3/CCL26 gene expression in eosinophilic esophagitis. - Rat Genome Database

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Treatment with topical steroids downregulates IL-5, eotaxin-1/CCL11, and eotaxin-3/CCL26 gene expression in eosinophilic esophagitis.

Authors: Lucendo, AJ  De Rezende, L  Comas, C  Caballero, T  Bellon, T 
Citation: Lucendo AJ, etal., Am J Gastroenterol. 2008 Sep;103(9):2184-93. doi: 10.1111/j.1572-0241.2008.01937.x.
RGD ID: 11081156
Pubmed: PMID:18844613   (View Abstract at PubMed)
DOI: DOI:10.1111/j.1572-0241.2008.01937.x   (Journal Full-text)

OBJECTIVES: Our aim was to evaluate the changes induced by topical steroid treatment to the esophageal epithelial inflammatory eosinophilic and T-cell infiltrate and to IL-5, eotaxin-1/CCL11, and eotaxin-3/CCL26 esophageal gene expression levels in patients with eosinophilic esophagitis (EE). METHODS: Esophageal biopsies were taken from eight adult patients at the moment of diagnosis and after 3-month treatment with fluticasone propionate. Eosinophils, CD8, and CD4 T cells were examined by immunohistochemistry. IL-5, eotaxin-1/CCL11, and eotaxin-3/CCL26 gene expression levels were measured by real-time PCR. Eight control samples were also analyzed. RESULTS: A significant decrease in the eosinophil infiltrate and in CD8(+) T-cell density was observed in the esophageal epithelium from the patients upon steroid treatment. IL-5 was not detected in control samples, and expression levels were variably downregulated after treatment in six of the patients. Gene expression of eotaxin-1/CCL11 showed relevant downregulation in four cases and a modest twofold decrease in three of the patients studied. Mean CCL11 expression values upon steroid treatment were similar to control samples (19.4 +/- 28.6 vs 8.42 +/- 5, P= 0.7). Eotaxin-3/CCL26 gene expression levels were significantly increased in EE. Although they were significantly downregulated upon steroid treatment, control expression levels were not reached in any of the cases analyzed (580.9 +/- 943.9 vs 1.45 +/- 1.0, P= 0.001). CONCLUSIONS: Our results confirm that eotaxin-3/CCL26 is significantly increased in EE esophageal samples. However, the individual analysis of IL-5, CCL11, and CCL26 expression data suggests that several cytokines and chemokines could participate in the physiopathology of EE in humans.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
eosinophilic esophagitis treatmentIDA 11081156 RGD 
eosinophilic esophagitis treatmentISOCCL26 (Homo sapiens)11081156; 11081156 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Ccl26  (C-C motif chemokine ligand 26)

Genes (Mus musculus)
Ccl26  (C-C motif chemokine ligand 26)

Genes (Homo sapiens)
CCL26  (C-C motif chemokine ligand 26)


Additional Information