ArticlePloS one2015
Humoral immunity links Candida albicans infection and celiac disease.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
- Coeliac disease and microbiota: is it time for personalised biotics intervention? A scoping review.BMJ nutrition, prevention & health · 2025Article
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- The immune and microbial homeostasis determines theLife science alliance · 2024Article
- Non-Host Factors Influencing Onset and Severity of Celiac Disease.Gastroenterology · 2024Review
- Association of gut microbiota with lactose intolerance and coeliac disease: a two-sample Mendelian randomization study.Frontiers in nutrition · 2024Article
- Advances in Understanding the Human Gut Microbiota and Its Implication in Pediatric Celiac Disease-A Narrative Review.Nutrients · 2023Review
- Article
- Fungal Dysbiosis in Children with Celiac Disease.Digestive diseases and sciences · 2022Article
- Viral dysbiosis in children with new-onset celiac disease.PloS one · 2022Article
- The Role of B-Cells and Antibodies againstVaccines · 2021Review
- Contribution of Infectious Agents to the Development of Celiac Disease.Microorganisms · 2021Review
- Molecular Biomarkers for Celiac Disease: Past, Present and Future.International journal of molecular sciences · 2020Review
- Gut microbiota in Celiac Disease: microbes, metabolites, pathways and therapeutics.Expert review of clinical immunology · 2020Review
- Bio- and Nanotechnology as the Key for Clinical Application of Salivary Peptide Histatin: A Necessary Advance.Microorganisms · 2020Review
- Processed Food Additive Microbial Transglutaminase and Its Cross-Linked Gliadin Complexes Are Potential Public Health Concerns in Celiac Disease.International journal of molecular sciences · 2020Review
- Celiac Disease and the Microbiome.Nutrients · 2019Review
- The Revival of the Battle between David and Goliath in the Enteric Viruses and Microbiota Struggle: Potential Implication for Celiac Disease.Microorganisms · 2019Review
- To Be or Not to Be a Pathogen:Frontiers in immunology · 2019Review
- IL-9 and Mast Cells Are Key Players of Candida albicans Commensalism and Pathogenesis in the Gut.Cell reports · 2018Article
- Microbial Transglutaminase Is Immunogenic and Potentially Pathogenic in Pediatric Celiac Disease.Frontiers in pediatrics · 2018Review
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe protein Hwp1, expressed on the pathogenic phase of Candida albicans, presents sequence analogy with the gluten protein gliadin and is also a substrate for transglutaminase. This had led to the suggestion that C. albicans infection (CI) may be a triggering factor for Celiac disease (CeD) onset. We investigated cross-immune reactivity between CeD and CI.
methodsSerum IgG levels against recombinant Hwp1 and serological markers of CeD were measured in 87 CeD patients, 41 CI patients, and 98 healthy controls (HC). IgA and IgG were also measured in 20 individuals from each of these groups using microchips sensitized with 38 peptides designed from the N-terminal of Hwp1.
resultsCI and CeD patients had higher levels of anti-Hwp1 (p=0.0005 and p=0.004) and anti-gliadin (p=0.002 and p=0.0009) antibodies than HC but there was no significant difference between CeD and CI patients. CeD and CI patients had higher levels of anti-transglutaminase IgA than HC (p=0.0001 and p=0.0039). During CI, the increase in anti-Hwp1 paralleled the increase in anti-gliadin antibodies. Microchip analysis showed that CeD patients were more reactive against some Hwp1 peptides than CI patients, and that some deamidated peptides were more reactive than their native analogs. Binding of IgG from CeD patients to Hwp1 peptides was inhibited by γIII gliadin peptides.
conclusionsHumoral cross-reactivity between Hwp1 and gliadin was observed during CeD and CI. Increased reactivity to Hwp1 deamidated peptide suggests that transglutaminase is involved in this interplay. These results support the hypothesis that CI may trigger CeD onset in genetically-susceptible individuals.
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