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Topical Corticosteroids Do Not Revert the Activated Phenotype of Eosinophils in Eosinophilic Esophagitis but Decrease Surface Levels of CD18 Resulting in Diminished Adherence to ICAM-1, ICAM-2, and Endothelial Cells

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Abstract

Swallowed topical corticosteroids are the standard therapy for eosinophilic esophagitis (EoE) in adults. Eosinophils in the blood of untreated EoE patients have an activated phenotype. Our aim was to determine if corticosteroids restore the phenotype of eosinophils to a healthy phenotype and if certain cell-surface molecules on blood eosinophils correlate with eosinophilic infiltration of the esophagus. Levels of eight surface markers on eosinophils from treated and untreated EoE patients were determined by flow cytometry and analyzed using multivariate methods of pattern recognition. Corticosteroid-treated EoE patients’ eosinophils had decreased levels of CD18 compared to both untreated patients and healthy controls, but maintained their activated phenotype. CD18 expression correlated positively with eosinophil numbers in the esophagus and promoted the adherence of eosinophils to ICAM-1, ICAM-2, and to endothelial cells. The diminished expression of CD18 may be one mechanism behind the reduced entry of eosinophils into the esophagus in corticosteroid-treated EoE patients.

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Acknowledgments

This work was funded by grants from the Swedish Research Council (K2010-57X-14180-09-3), LUA-ALF (71580), Cancer and Allergy Foundation, Health & Medical Care Committee of the Regional Executive Board of Region Västra Götaland (96490), Inga Britt and Arne Lundberg Research Foundation, and University of Gothenburg.

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None of the authors has any potential financial conflict of interest related to this manuscript.

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Correspondence to Christine Lingblom.

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Christine Lingblom and Henrik Bergquist contributed equally to this study.

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Lingblom, C., Bergquist, H., Johnsson, M. et al. Topical Corticosteroids Do Not Revert the Activated Phenotype of Eosinophils in Eosinophilic Esophagitis but Decrease Surface Levels of CD18 Resulting in Diminished Adherence to ICAM-1, ICAM-2, and Endothelial Cells. Inflammation 37, 1932–1944 (2014). https://doi.org/10.1007/s10753-014-9926-x

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