ArticleHuman molecular genetics2014
Coregulation and modulation of NFκB-related genes in celiac disease: uncovered aspects of gut mucosal inflammation.
Article in Human molecular genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 82 citations in OpenAlex.
- Comparison of DNA methylation profiles from saliva in Coeliac disease and non-coeliac disease individuals.BMC medical genomics · 2020Trial
- Trial
- The long noncoding RNA lnc13 restrains inflammatory responses to maintain oral tolerance to gluten.Nature immunology · 2026Article
- Review
- Diagnosis of celiac disease on a gluten-free diet: a multicenter prospective quasi-experimental clinical study.BMC medicine · 2025Article
- Sustainable milk-based postbiotics beverages fermented byFrontiers in nutrition · 2025Article
- Potential of nutraceuticals in celiac disease.Tissue barriers · 2025Review
- mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Roles of lncRNAs in NF-κB-Mediated Macrophage Inflammation and Their Implications in the Pathogenesis of Human Diseases.International journal of molecular sciences · 2024Review
- Ex vivo gliadin stimulation of intestinal cells.Methods in cell biology · 2023Article
- Functional implications of the CpG island methylation in the pathogenesis of celiac disease.Molecular biology reports · 2022Review
- Pivotal Role of Inflammation in Celiac Disease.International journal of molecular sciences · 2022Review
- Inflammation Is Present, Persistent and More Sensitive to Proinflammatory Triggers in Celiac Disease Enterocytes.International journal of molecular sciences · 2022Article
- Celiac disease: From genetics to epigenetics.World journal of gastroenterology · 2022Review
- Gluten-induced RNA methylation changes regulate intestinal inflammation via allele-specificGut · 2022Article
- Why are western diet and western lifestyle pro-inflammatory risk factors of celiac disease?Frontiers in nutrition · 2022Review
- Single-Cell RNA Sequencing of Peripheral Blood Mononuclear Cells From Pediatric Coeliac Disease Patients Suggests Potential Pre-Seroconversion Markers.Frontiers in immunology · 2022Article
- A Novel Regulatory Player in the Innate Immune System: Long Non-Coding RNAs.International journal of molecular sciences · 2021Review
- Mitigation of Gliadin-Induced Inflammation and Cellular Damage by Curcumin in Human Intestinal Cell Lines.Inflammation · 2021Article
- Potential impact of celiac disease genetic risk factors on T cell receptor signaling in gluten-specific CD4+ T cells.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is known that the NFκB route is constitutively upregulated in celiac disease (CD), an immune-mediated disorder of the gut caused by intolerance to ingested gluten. Our aim was to scrutinize the expression patterns of several of the most biologically relevant components of the NFκB route in intestinal biopsies from active and treated patients and after in vitro gliadin challenge, and to assess normalization of the expression using an inhibitor of the MALT1 paracaspase. The expression of 93 NFκB genes was measured by RT-PCR in a set of uncultured active and treated CD and control biopsies, and in cultured biopsy series challenged with gliadin, the NFκB modulator, both compounds and none. Methylation of eight genes involved in NFκB signaling was analyzed by conventional pyrosequencing. Groups were compared and Pearson's correlation matrixes were constructed to check for coexpression and co-methylation. Our results confirm the upregulation of the NFκB pathway and show that constitutively altered genes usually belong to the core of the pathway and have central roles, whereas genes overexpressed only in active CD are more peripheral. Additionally, this is the first work to detect methylation level changes in celiac intestinal mucosa. Coexpression is very common in controls, whereas gliadin challenge and especially chronic inflammation present in untreated CD result in the disruption of the regulatory equilibrium. In contrast, co-methylation occurs more often in active CD. Importantly, NFκB modulation partially restores coregulation, opening the door to future therapeutic possibilities and targets.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.