ArticleCellular and molecular gastroenterology and hepatology2016
NOD-Like Receptor Protein 3 Inflammasome Priming and Activation in Barrett's Epithelial Cells.
Article in Cellular and molecular gastroenterology and hepatology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Gastrointestinal microbiota alterations associated with pediatric gastroesophageal reflux disease and proton pump inhibitor exposure: a systematic review of microbiome changes, dysbiosis markers, and associated clinical outcomes.Frontiers in nutrition · 2026Pooled it
- Relationship of the Esophageal Microbiome and Tissue Gene Expression and Links to the Oral Microbiome: A Randomized Clinical Trial.Clinical and translational gastroenterology · 2020Trial
- Review
- Cell membrane-encased thylakoid as white light triggered PDT therapy for facile and targeted choroidal melanoma treatment.Bioactive materials · 2026Article
- Review
- Multi-Cohort Transcriptomics Combined with Mendelian Randomization Identifies PPARGC1A, NAAA and GIPC2 as NLRP3 Inflammasome-Related Key Genes in Ulcerative Colitis.Journal of inflammation research · 2026Article
- Pyroptosis-immunity-microbiome axis in acute upper gastrointestinal bleeding: mechanisms, risk prediction, and individualized strategies.Frontiers in medicine · 2026Review
- Geranylgeranoic acid, toll-like receptor 4, and pyroptosis-related signaling in hepatocellular carcinoma: a hypothesis-generating perspective.Oncology reviews · 2026Article
- Intestinal and esophageal microbiota in esophageal cancer development and treatment.Gut microbes · 2025Review
- Amprenavir Mitigates Pepsin-Induced Transcriptomic Changes in Normal and Precancerous Esophageal Cells.International journal of molecular sciences · 2025Article
- Investigation of the mechanism by which miR-223-3p inhibits reflux esophagitis through targeting the NLRP3 inflammasome.BMC gastroenterology · 2025Article
- Targeting pyroptosis for cancer immunotherapy: mechanistic insights and clinical perspectives.Molecular cancer · 2025Review
- Exosomal Drug Delivery Systems: A Novel Therapy Targeting PD-1 in Septic-ALI.Stem cell reviews and reports · 2024Article
- Altered Microbiome Promotes Pro-Inflammatory Pathways in Oesophago-Gastric Tumourigenesis.Cancers · 2024Review
- Palmitoylethanolamide (PEA) for Prevention of Gastroesophageal Inflammation: Insights from In Vitro Models.Life (Basel, Switzerland) · 2024Article
- Britannilactone 1-O-acetate induced ubiquitination of NLRP3 inflammasome through TRIM31 as a protective mechanism against reflux esophagitis-induced esophageal injury.Chinese medicine · 2024Article
- Investigating the causal relationship of gut microbiota with GERD and BE: a bidirectional mendelian randomization.BMC genomics · 2024Article
- From microbes to medicine: harnessing the power of the microbiome in esophageal cancer.Frontiers in immunology · 2024Review
- Exploring the role of pyroptosis in the pathogenicity of heart disease.Frontiers in physiology · 2024Review
- Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsMicrobial molecular products incite intestinal inflammation by activating Toll-like receptors (TLRs) and inflammasomes of the innate immune system. This system's contribution to esophageal inflammation is not known. Gram-negative bacteria, which dominate the esophageal microbiome in reflux esophagitis, produce lipopolysaccharide (LPS), a TLR4 ligand. TLR4 signaling produces pro-interleukin (IL)1β, pro-IL18, and NOD-like receptor protein 3 (NLRP3), which prime the NLRP3 inflammasome. Subsequent NLRP3 inflammasome activation cleaves caspase-1, inducing secretion of proinflammatory cytokines and pyroptosis (inflammatory cell death). We explored LPS effects on NLRP3 inflammasome priming and activation in esophageal cells.
methodsWe exposed esophageal squamous and Barrett's epithelial cells to LPS and measured the following: (1) TLR4, pro-IL1β, pro-IL18, and NLRP3 expression; (2) caspase-1 activity; (3) tumor necrosis factor-α, IL8, IL1β, and IL18 secretion; (4) lactate dehydrogenase (LDH) release (a pyroptosis marker); and (5) mitochondrial reactive oxygen species (ROS). As inhibitors, we used acetyl-Tyr-Val-Ala-Asp-CHO for caspase-1, small interfering RNA for NLRP3, and (2-(2,2,6,6,-Tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl)triphenylphosphonium chloride for mitochondrial ROS.
resultsSquamous and Barrett's cells expressed similar levels of TLR4, but LPS induced TLR4 signaling that increased tumor necrosis factor-α and IL8 secretion only in Barrett's cells. Barrett's cells treated with LPS showed increased expression of pro-IL18, pro-IL1β, and NLRP3, and increased mitochondrial ROS levels, caspase-1 activity, IL1β and IL18 secretion, and LDH release. Acetyl-Tyr-Val-Ala-Asp-CHO, NLRP3 small interfering RNA, and Mito-TEMPO all blocked LPS-induced IL1β and IL18 secretion and LDH release.
conclusionsIn Barrett's cells, LPS both primes and activates the NLRP3 inflammasome, causing secretion of proinflammatory cytokines and pyroptosis. By triggering molecular events promoting inflammation, the esophageal microbiome might contribute to inflammation-mediated carcinogenesis in Barrett's esophagus.
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