ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Lipopolysaccharide Regulation of Intestinal Tight Junction Permeability Is Mediated by TLR4 Signal Transduction Pathway Activation of FAK and MyD88.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 201 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
201 citing papers in PubMed, 2 syntheses or guidelines pooled it, 401 citations in OpenAlex.
- Gut microbiota and ALS: cause, consequence or correlation? - a systematic review.Frontiers in neuroscience · 2026Pooled it
- Diagnostic, prognostic, and therapeutic potentials of gut microbiome profiling in human schistosomiasis: A comprehensive systematic review.PLoS neglected tropical diseases · 2025Pooled it
- Review
- Reduced gut microbiota-derived indole-3-carboxaldehyde and 5-hydroxyindole-3-acetic acid are associated with intestinal barrier dysfunction and inflammation in diarrheic suckling lambs.Journal of animal science and biotechnology · 2026Article
- Salicifoliosides A and B: A Pair of Furan Glycoside Isomers From Chimonanthus salicifolius and Their Modulation of the Functions of Caco-2 Cells.Chemistry & biodiversity · 2026Article
- A Comprehensive Review on Irinotecan-Induced Delayed Diarrhea: From Mechanisms to Therapeutic Options.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Integrated bioinformatics and experimental validation reveal that kaempferol ameliorates intervertebral disc degeneration via dual anti-inflammatory and anti-aging pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Effects of tea polyphenols on intestinal barrier, antioxidant capacity, and cecal microbiota in lion-head geese.Poultry science · 2026Article
- Context-dependent release of HMGB1: cell death mode, cell type and LPS stress drive monomer and heterocomplex formation.Molecular medicine (Cambridge, Mass.) · 2026Article
- Gut Microbiota, Diet and Lipid Metabolism in Adolescents with NAFLD and Their Role in Preventive Strategies.International journal of molecular sciences · 2026Review
- Targeting Gut Dysbiosis and Short-Chain Fatty Acid Deficiency in Chronic Eczema: A Case Report.Integrative medicine (Encinitas, Calif.) · 2026Article
- Screening of Lactobacillus plantarum LPH10 and Its Anti-inflammatory Properties: Acid and Bile Salt Tolerance, Bacteriostatic Activity and Regulation of NF-κB/IRF Pathways.Probiotics and antimicrobial proteins · 2026Article
- Evaluation Profile of SicilianPlants (Basel, Switzerland) · 2026Article
- Probiotic bacteria Bifidobacterium bifidum upregulation of intestinal epithelial tight junction barrier is mediated by TLR-2/TLR-6 receptor complex activation of occludin gene.NPJ biofilms and microbiomes · 2026Article
- Molecular Mechanisms of Lignans in Lowering Blood Pressure and Anti-Obesity Effects: A Review.Foods (Basel, Switzerland) · 2026Review
- The role of NLRP3 inflammasome in necrotizing enterocolitis.Pediatric research · 2026Review
- Gut microbiota-liver-kidney axis in diabetic kidney disease: mechanistic insights into amino acid metabolism and nutritional intervention strategies targeting natural bioactive compounds.Frontiers in nutrition · 2026Review
- Intestinal permeability and the zonulin pathway: tight junctions, mucosal immunity, dietary modulators and clinical relevance.Frontiers in nutrition · 2026Review
- Shotgun metagenomic analysis reveals taxonomic and functional alterations in the gut microbiome across prodromal and symptomatic Lewy body disease.Frontiers in microbiomes · 2026Article
- The role of gut microbiome disruption in the development of metabolic dysfunction-associated kidney disease.Acta biochimica Polonica · 2026Review
141 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Gut-derived bacterial LPS plays an essential role in inducing intestinal and systemic inflammatory responses and have been implicated as a pathogenic factor in necrotizing enterocolitis and inflammatory bowel disease. The defective intestinal tight junction barrier was shown to be an important factor contributing to the development of intestinal inflammation. LPS, at physiological concentrations, causes an increase in intestinal tight junction permeability (TJP) via a TLR4-dependent process; however, the intracellular mechanisms that mediate LPS regulation of intestinal TJP remain unclear. The aim of this study was to investigate the adaptor proteins and the signaling interactions that mediate LPS modulation of intestinal tight junction barrier using in vitro and in vivo model systems. LPS caused a TLR4-dependent activation of membrane-associated adaptor protein focal adhesion kinase (FAK) in Caco-2 monolayers. LPS caused an activation of both MyD88-dependent and -independent pathways. Small interfering RNA silencing of MyD88 prevented an LPS-induced increase in TJP. LPS caused MyD88-dependent activation of IL-1R-associated kinase 4. TLR4, FAK, and MyD88 were colocalized. Small interfering silencing of TLR4 inhibited TLR4-associated FAK activation, and FAK knockdown prevented MyD88 activation. In vivo studies also confirmed that the LPS-induced increase in mouse intestinal permeability was associated with FAK and MyD88 activation; knockdown of intestinal epithelial FAK prevented an LPS-induced increase in intestinal permeability. Additionally, high-dose LPS-induced intestinal inflammation was dependent on the TLR4/FAK/MyD88 signal transduction axis. To our knowledge, our data show for the first time that the LPS-induced increases in intestinal TJP and intestinal inflammation were regulated by TLR4-dependent activation of the FAK/MyD88/IL-1R-associated kinase 4 signaling pathway.
Indexed as
Identifiers
What OpenQuestion holds
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.