ReviewDigestive diseases and sciences2026
Deciphering the TLR4 and NLRP3 Inflammasome Crosstalk for Therapeutic Restoration of Intestinal and Systemic Immunity.
Review in Digestive diseases and sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
The trial behind it
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Who cites it
6 citing papers in PubMed.
- Review
- Review
- The Paradoxical Role of Pyroptosis in Gastrointestinal Cancers: From Molecular Mechanisms to Therapeutic Horizons.Biomedicines · 2026Review
- Article
- The Gut Microbiota-NLRP3 Inflammasome Axis in Chronic Heart Failure: Mechanisms Across Heart Failure Phenotypes and Therapeutic Perspectives.Journal of inflammation research · 2026Review
- Loss of immunometabolic adaptability in MASH: gut-derived signals drive macrophage reprogramming and fibrosis.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe gastrointestinal (GI) tract is a highly immunologically active organ where coordinated crosstalk between Toll-like receptor 4 (TLR4) and NLRP3 inflammasome maintains epithelial integrity, supports mucosal repair, and promotes immune tolerance. This review aims to summarize current understanding of TLR4-NLRP3 interactions in the gut, examine their in disease, examine their roles in disease, and evaluate emerging therapeutic strategies targeting this axis.
methodsA comprehensive review of recent literature was conducted, focusing on regulatory mechanisms governing TLR4-NLRP3 signaling under homeostasis and dysregulation. Studies addressing epithelial barrier function, cytokine signaling, pyroptosis, metabolic endotoxemia, dysbiosis, and gut-brain axis communication were examined. Research using organoids, gut-on-chip system, microbiota modulation, and multi-omics approaches was also evaluated to understand therapeutic and translational advancements.
resultsFindings indicate that balanced TLR4-NLRP3 signaling preserves epithelial barrier integrity, regulates inflammatory responses, and supports immunological tolerance. Dysregulation disrupts these protective mechanisms and initiates feed-forward cycle of epithelial damage, metabolic endotoxemia, dysbiosis, and heightened cytokine-driven inflammation. Such aberrant activity contributes to major intestinal diseases-including inflammatory bowel disease, necrotizing enterocolitis, and colorectal cancer-as well as extraintestinal conditions such as obesity, type 2 diabetes, and neuroinflammation through gut-brain axis pathways. Novel therapeutic strategies, including selective small-molecule inhibitors and microbiota-based interventions, show potential for targeted modulation.
conclusionThe TLR4-NLRP4 axis is a context-dependent regulator of gut and systemic immunity. Targeted modulation of this pathway represents a promising strategy to restore immune homeostasis while preserving host defense, supporting its relevance as a translational therapeutic target across multiple immune-mediated disorders.
Indexed as
Identifiers
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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.