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

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
CCL26Humaneosinophilic esophagitis treatmentIDA  RGD 
Ccl26Rateosinophilic esophagitis treatmentISOCCL26 (Homo sapiens) RGD 
Ccl26Mouseeosinophilic esophagitis treatmentISOCCL26 (Homo sapiens) 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