4.4 Article

Distinctive Blood Eosinophilic Phenotypes and Cytokine Patterns in Eosinophilic Esophagitis, Inflammatory Bowel Disease and Airway Allergy

期刊

JOURNAL OF INNATE IMMUNITY
卷 3, 期 6, 页码 594-604

出版社

KARGER
DOI: 10.1159/000331326

关键词

Cytokines; Eosinophils; Inflammatory bowel disease; Eosinophilic esophagitis; Flow cytometry

资金

  1. Swedish Research Council [K2010-57X-14180-09-3]
  2. LUA-ALF [71580]
  3. Cancer and Allergy Foundation
  4. Health and Medical Care Committee of the Regional Executive Board of Region Vastra Gotaland [96490]
  5. Council Th. Bergh Foundation
  6. Inga-Britt and Arne Lundberg Research Foundation

向作者/读者索取更多资源

Blood eosinophil numbers may be elevated in allergy, inflammatory bowel disease and eosinophilic esophagitis. The aim of this study was to examine whether circulating eosinophils display distinct phenotypes in these disorders and if different patterns of eosinophilic chemoattractants exist. Blood eosinophils from patients with symptomatic eosinophilic esophagitis (EoE; n = 12), ulcerative colitis (n = 8), airway allergy (n = 10) and healthy controls (n = 10) were enumerated and their surface markers analyzed by flow cytometry. Plasma levels of pro-eosinophilic cytokines were quantified in parallel. Data were processed by multivariate pattern recognition methods to reveal disease-specific patterns of eosinophil phenotypes and cytokines. EoE patients had higher numbers of eosinophils with enhanced expression of CD23, CD54, CRTH2 and CD11c and diminished CCR3 and CD44 expression. Plasma CCL5 was also increased in EoE. Although allergic patients had increased interleukin (IL)-2, IL-3, IL-5 and granulocyte macrophage colony-stimulating factor plasma concentrations, their blood eosinophil phenotypes were indistinguishable from those of healthy controls. Decreased eosinophilic expression of CD11b, CD18, CD44 and CCR3, but no distinctive pattern of eosinophil chemoattractants, characterized ulcerative colitis. We propose that eosinophils acquire varying functional properties as a consequence of distinct patterns of activation signals released from the inflamed tissues in different diseases. Copyright (C) 2011 S. Karger AG, Basel

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