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Identification of celiac-disease active peptides in gluten-free beers by nanoLC-MS/MS

ABSTRACT: Barley beers may be rendered gluten-free by specialized brewing processes. One controversial issue is whether these beers contain residual gluten peptides carrying at least one celiac disease (CeD)-active epitope, because routine methods to assess whether the beer is gluten-free like competitive enzyme-linked immunosorbent assays (ELISA) may fail to detect potentially harmful peptides. We used untargeted nano-liquid chromatography-tandem mass spectrometry (nanoLC MS/MS) to identify CeD-active peptides in 21 gluten-free barley beers and four regular or carbohydrate-reducedbeers. While the G12 ELISA confirmed gluten levels below 20 mg/kg in all gluten-free beers, the R5 ELISA detected gluten levels in four beers exceeding this threshold, highlighting method discrepancies. nanoLC-MS/MS identified 44 CeD active peptides in seven gluten-free and four non-gluten-free beers, of which 17 CeD-active peptides had no ELISA epitope and therefore escape detection. Accurate quantitation of thesepeptides combined with in vivo toxicity assessment will be needed to provide guidance on clinical relevance.

INSTRUMENT(S):

ORGANISM(S): Hordeum Vulgare (barley) Triticum Aestivum (wheat)

DISEASE(S): Celiac Disease

SUBMITTER: Eleonora Tissen

LAB HEAD: Katharina Scherf

PROVIDER: PXD059719 | Pride | 2026-04-01

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	RESULTS_TXT_MQ_runs.zip	Other
	allBeers.RAW.zip	Raw
	checksum.txt	Txt

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Project description:Coeliac Disease (CeD) is a chronic autoimmune disorder affecting 0.5-1% of the general population with a wide geographical distribution. Despite recent efforts to deeply phenotype gluten-specific immune activation at the single cell level, recent clinical studies targeting gluten degradation and other immune tolerance mechanisms have been unsuccessful. To this end, a deeper understanding of immune and non-immune cellular dynamics and interactions are required to characterize tissue-specific mechanisms responsible for CeD pathogenesis, repair, and resolution. Here, we assembled the most comprehensive scRNAseq dataset in Coeliac Disease to date, including 203,555 cells across 21 active CeD and 11 control duodenal samples. Compared to control duodenum, CeD was characterized by single cell differential changes in abundance, gene expression and cell-cell interactions across cellular compartments. In the immune compartments, CeD samples showed expected increases in plasma cell abundance and shifts toward type 1 effector biology (e.g., increase in cycling CD8pos, γδ T cells and IFNG transcriptional shifts) and Tfh-related biology (e.g., increases in IL21 signaling to effector T cells). In addition, activated myeloid subsets, including DC2 and monocytes, were increased in disease and were characterized by increased pro-inflammatory pathway expression, including IL-1β. Non-immune compartments showed increased stem/crypt and secretory enterocytes in CeD samples with a decrease in absorptive enterocytes, reflecting the villus atrophy and crypt hyperplasia hallmarks of CeD epithelial dysfunction. Accompanying the epithelial changes, distinct changes in stromal populations were identified, particularly with increases in abundance and transcriptional activity of NRG1 and SMOC2 fibroblasts. Cell-cell interaction analysis across multiple cellular compartments proposed a distinct increased role of fibroblasts to support the epithelial reprogramming of the increased stem/crypt epithelial fraction in CeD, mediated by myeloid derived IL-1β signal and lymphoid-derived IFN-γ. This dataset reveals a previously unknown role for T-myeloid-stromal-epithelial cell communication in CeD, highlighting key mechanisms of the tissue-level cellular dynamics in response to gluten ingestion.

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Identification of celiac-disease active peptides in gluten-free beers by nanoLC-MS/MS

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