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Elaine L. Leonard Puppa

Researcher at University of Maryland, Baltimore

Publications -  10
Citations -  934

Elaine L. Leonard Puppa is an academic researcher from University of Maryland, Baltimore. The author has contributed to research in topics: Gliadin & Gluten. The author has an hindex of 6, co-authored 9 publications receiving 837 citations.

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Natural history of celiac disease autoimmunity in a USA cohort followed since 1974

TL;DR: The CLUE study demonstrated that this increase in CD prevalence increased 2-fold in the CLUE cohort and 5-fold overall in the US since 1974 was due to an increasing number of subjects that lost the immunological tolerance to gluten in their adulthood.
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Proof of Concept of Microbiome-Metabolome Analysis and Delayed Gluten Exposure on Celiac Disease Autoimmunity in Genetically At-Risk Infants

TL;DR: It is shown that infants genetically susceptible to CD who are exposed to gluten early mount an immune response against gluten and develop CD autoimmunity more frequently than at-risk infants in which gluten exposure is delayed until 12 months of age.
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Effect of gliadin on permeability of intestinal biopsy explants from celiac disease patients and patients with non-celiac gluten sensitivity.

TL;DR: Following gliadin exposure, both patients with gluten sensitivity and those with active celiac disease demonstrate a greater increase in intestinal permeability than celiacs in disease remission.
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Trace gluten contamination may play a role in mucosal and clinical recovery in a subgroup of diet-adherent non-responsive celiac disease patients

TL;DR: The GCED may be an effective therapeutic option for GFD-adherent NRCD patients and identifies a subgroup of patients, previously classified as RCD1, that is not truly refractory to dietary treatment.
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Identification of a novel immunomodulatory gliadin peptide that causes interleukin-8 release in a chemokine receptor CXCR3-dependent manner only in patients with coeliac disease

TL;DR: Induction of IL‐8 was reproduced by one of a comprehensive panel of synthetic α‐gliadin peptides and was abrogated when CXCR3 was blocked before stimulation with either gliadin or this peptide in the CD group but not in the control group, suggesting thatgliadin‐induced IL-8 production was CX CR3‐dependent gliaddin induced IL‐ 8 production only in CD.