Abstract
BackgroundIn contrast to the well-characterized Celiac Disease (CD), the clinical scenarios encompassed by the non-celiac self-reported wheat sensitivity (NCSRWS) might be related to different antigens that trigger distinct immune-inflammatory reactions. Although an increased number of intestinal intraepithelial lymphocytes is observed at the inception of both diseases, the subsequent immunopathogenic pathways seem to be different. We aimed to describe the cytokine profile observed in the duodenal mucosa of patients with NCSRWS.MethodsIn a blind, cross-sectional study, we included duodenal biopsies from 15 consecutive untreated patients with active CD, 9 individuals with NCSRWS and 10 subjects with dyspepsia without CD and food intolerances. Immunohistochemistry and flow-cytometry were used to determine the presence of pro-inflammatory cytokine expressing monocytes and monocyte-derived dendritic cells involved in innate immune activation, cytokine-driven polarization and maintenance of Th1 and Th17/Th 22, and anti-inflammatory/profibrogenic cytokines.ResultsThe percentage of cells expressing all tested cytokines in the lamina propria and the epithelium was higher in CD patients than in the control group. Cytokines that induce and maintain Th1 and Th17 polarization were higher in CD than in NCSRWS and controls, also were higher in NCSRWS compared to controls. Similar differences were detected in the expression of IL-4 and TGF-1, while IL-10-expressing cells were lower in NCSRWS patients than in controls and CD subjects.ConclusionsNCSRWS patients exhibit components of both, innate and adaptive immune mechanisms but to a lesser extent compared to CD.
Highlights
In contrast to the well-characterized Celiac Disease (CD), the clinical scenarios encompassed by the non-celiac self-reported wheat sensitivity (NCSRWS) might be related to different antigens that trigger distinct immune-inflammatory reactions
The ingestion of gluten and related proteins triggers well known immunopathogenic mechanisms orchestrated by CD4+ T helper 1 (Th1) and T helper 17 lymphocytes (Th17) cells that result in mucosal inflammation and villus atrophy (VA) [7,8,9,10,11,12]
Certain components of adaptive immunity may be involved [21,22,23]. In this exploratory study we aimed to describe the cytokine profile and quantify the pro-inflammatory cytokine-expressing monocyte and monocyte-derived dendritic cells involved in innate immune activation, cytokine-driven polarization and maintenance of Th1 polarization and Th17/T helper 22 lymphocytes (Th22), and anti-inflammatory/ profibrogenic cytokines in the duodenal mucosa of a group of subjects with self-reported wheat sensitivity
Summary
In contrast to the well-characterized Celiac Disease (CD), the clinical scenarios encompassed by the non-celiac self-reported wheat sensitivity (NCSRWS) might be related to different antigens that trigger distinct immune-inflammatory reactions. Due to the lack of specific biomarkers, in patients with normal duodenal biopsies and negative CD serology, the diagnosis of NCGS is largely based upon complex and seldom performed clinical evaluations such as double-blind gluten-placebo challenge in which symptoms improve during a gluten-free diet and symptoms relapse once gluten ingestion is resumed. In these cases, wheat allergy should be ruled out [4,5,6]. NCGS is a poorly characterized disorder in which the role of gluten as the main antigen and the pathophysiologic mechanisms responsible for tissue damage and symptoms development is debatable [13]
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