Topical Corticosteroids Do Not Revert the Activated Phenotype of Eosinophils in Eosinophilic Esophagitis but Decrease Su
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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 Christine Lingblom,1,5 Henrik Bergquist,2 Marianne Johnsson,1 Patrik Sundström,3 Marianne Quiding-Järbrink,3 Mogens Bove,4 and Christine Wennerås1
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. KEY WORDS: adhesion; CD18; corticosteroids; eosinophils; eosinophilic esophagitis; ICAM.
INTRODUCTION Eosinophilic esophagitis (EoE) is a newly described disease [1] that mainly afflicts persons living in Westernized societies [2]. Difficulty in swallowing food and food impaction are the main symptoms in adults. EoE is believed to be a chronic antigen-driven inflammatory
Christine Lingblom and Henrik Bergquist contributed equally to this study. 1
Department of Infectious Diseases, Sahlgrenska Academy, Gothenburg University, Guldhedsgatan 10A, 41346 Göteborg, Sweden 2 Department of ENT, Head and Neck Surgery, Sahlgrenska Academy, Gothenburg University, Göteborg, Sweden 3 Department of Microbiology and Immunology, Sahlgrenska Academy, Gothenburg University, Göteborg, Sweden 4 Department of ENT, Head and Neck Surgery, NÄL Hospital, Trollhättan, Sweden 5 To whom correspondence should be addressed at Department of Infectious Diseases, Sahlgrenska Academy, Gothenburg University, Gu ldh eds ga tan 10A, 413 46 Gö teb org, Swe de n. E- ma il: [email protected]
process [3]. The identity of the triggering antigen is uncertain, although food and inhalant allergens have been implicated [4]. Whereas the esophagus of healthy individuals is devoid of eosinophils [5], infiltrating eosinophils are seen in EoE and constitute a diagnostic requirement [3]. Other typical histopathological findings in EoE are increased numbers of mast cells, CD8+ T cells, and B cells [6, 7]. An initial study indicated that reduction of eosinophil numbers in the esophagus via administration of anti-IL
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