Innate and adaptive immunity in self-reported nonceliac gluten sensitivity versus celiac disease

Research output: Contribution to journalArticlepeer-review

Abstract

Background: Immune mechanisms have been implicated in nonceliac gluten sensitivity (NCGS), a condition characterized by intestinal and/or extraintestinal symptoms caused by the ingestion of gluten in non-celiac/non-wheat allergic individuals. Aims: We investigated innate and adaptive immunity in self-reported NCGS versus celiac disease (CD). Methods: In the supernatants of ex vivo-cultured duodenal biopsies from 14 self-reported NCGS patients, 9 untreated and 10 treated CD patients, and 12 controls we detected innate cytokines - interleukin (IL)-15, tumor necrosis factor-α, IL-1β, IL-6, IL-12p70, IL-23, IL-27, IL-32α, thymic stromal lymphopoietin (TSLP), IFN-α-, adaptive cytokines - interferon (IFN)-γ, IL-17A, IL-4, IL-5, IL-10, IL-13-, chemokines - IL-8, CCL1, CCL2, CCL3, CCL4, CCL5, CXCL1, CXCL10-, granulocyte colony stimulating factor (G-CSF) and granulocyte-macrophage colony stimulating factor (GM-CSF). Results: Mucosal innate and adaptive cytokines, chemokines and growth factors did not differ between self-reported NCGS, treated CD and controls. On the contrary, IL-6, IL-15, IL-27, IFN-α, IFN-γ, IL-17A, IL-23, G-CSF, GM-CSF, IL-8, CCL1 and CCL4 were significantly higher in untreated CD than in self-reported NCGS, treated CD and controls, while TSLP was significantly lower in untreated CD than in self-reported NCGS, treated CD and controls. Conclusion: In our hands, patients with self-reported NCGS showed no abnormalities of the mucosal immune response.

Original languageEnglish
JournalDigestive and Liver Disease
DOIs
Publication statusAccepted/In press - Dec 13 2015

Keywords

  • Chemokine
  • Cytokine
  • Duodenal mucosa
  • Tissue transglutaminase

ASJC Scopus subject areas

  • Gastroenterology
  • Hepatology

Fingerprint Dive into the research topics of 'Innate and adaptive immunity in self-reported nonceliac gluten sensitivity versus celiac disease'. Together they form a unique fingerprint.

Cite this