Evidence map›Paper›PMID 41814048›Full record

ArticleMolecular and cellular pediatrics2026

Excessive poly(ADP)-ribosylation in the inflamed mucosa of pediatric celiac disease points to a novel inflammatory mechanism and therapeutic target.

Tala M Haddadin, Tarek M Masannat, Irshad A Sheikh, Belinda Sun, Connor P Kelley, Fayez K Ghishan, Pawel R Kiela

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Article in Molecular and cellular pediatrics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Tala M HaddadinDepartment of Pediatrics, Daniel Cracchiolo Institute for Pediatric Autoimmune Disease Research, Steele Children's Research Center, University of Arizona Health Sciences, Tucson, AZ, USA.
Tarek M MasannatDepartment of Pediatrics, Daniel Cracchiolo Institute for Pediatric Autoimmune Disease Research, Steele Children's Research Center, University of Arizona Health Sciences, Tucson, AZ, USA.
Irshad A SheikhDepartment of Pediatrics, Daniel Cracchiolo Institute for Pediatric Autoimmune Disease Research, Steele Children's Research Center, University of Arizona Health Sciences, Tucson, AZ, USA.
Belinda SunDepartment of Pathology, University of Arizona, Tucson, AZ, USA.
Connor P KelleyDepartment of Pediatrics, Daniel Cracchiolo Institute for Pediatric Autoimmune Disease Research, Steele Children's Research Center, University of Arizona Health Sciences, Tucson, AZ, USA.
Fayez K GhishanDepartment of Pediatrics, Daniel Cracchiolo Institute for Pediatric Autoimmune Disease Research, Steele Children's Research Center, University of Arizona Health Sciences, Tucson, AZ, USA.
Pawel R KielaDepartment of Pediatrics, Daniel Cracchiolo Institute for Pediatric Autoimmune Disease Research, Steele Children's Research Center, University of Arizona Health Sciences, Tucson, AZ, USA. pkiela@arizona.edu.ORCID http://orcid.org/0000-0002-0014-3517

Funding

NIDDK NIH HHS 5R01DK136240
6 · The paper itself

Abstract

backgroundCeliac disease (CD) is an immune-mediated enteropathy triggered by gluten exposure in genetically susceptible individuals, characterized by chronic intestinal inflammation, epithelial damage, and immune dysregulation. Several programmed cell death pathways have been implicated in CD pathogenesis, including apoptosis and pro-inflammatory pathways of programmed cell death, such as pyroptosis and necroptosis. HYPOTHESIS: Parthanatos - a caspase-independent, inflammatory cell death pathway mediated by poly(ADP-ribose) polymerases (PARP-1/2) and excessive poly(ADP)-ribosylation (PARylation), also contributes to epithelial cell death in CD.

methodsDuodenal and bulb biopsies from 15 pediatric patients with biopsy-confirmed CD and 15 non-CD controls were analyzed using immunofluorescence staining for poly(ADP-ribose) (PARylation) and CD3+ T cell infiltration.

resultsCD biopsies from duodenum and duodenal bulb demonstrated pathological hyperPARylation (p<0.001) and CD3+ T cell infiltration (p<0.001) compared to non-CD controls. HyperPARylation was evident both in epithelial and subepithelial compartments of the inflamed mucosa and was positively correlated with Marsh scoring criteria.

conclusionsOur findings identify mucosal hyperPARylation as a novel feature of the inflamed mucosa in pediatric CD, supporting a potential role for Parthanatos in mucosal injury and amplification of inflammatory responses. This opens new avenues for therapeutic exploration, including PARP inhibition, particularly in refractory CD.

Indexed as

Celiac diseaseDuodenumPARP1PARylationpoly(ADP-ribosylation)

Identifiers

PMID41814048
PMCPMC12979736

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