ArticleJournal of immunology (Baltimore, Md. : 1950)2008
TLR2 regulates gap junction intercellular communication in airway cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
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.
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Who cites it
31 citing papers in PubMed, 56 citations in OpenAlex.
- Cell type-specific interactions induce tonic interferon production in endothelial cells in a pathogen-independent manner.Cell communication and signaling : CCS · 2026Article
- Intercellular Communication in Airway Epithelial Cell Regeneration: Potential Roles of Connexins and Pannexins.International journal of molecular sciences · 2023Review
- A succinate/SUCNR1-brush cell defense program in the tracheal epithelium.Science advances · 2023Article
- Rhinovirus C causes heterogeneous infection and gene expression in airway epithelial cell subsets.Mucosal immunology · 2023Article
- The Role of Connexin 43 in Lung Disease.Life (Basel, Switzerland) · 2020Review
- The effects of genotype × phenotype interactions on silver nanoparticle toxicity in organotypic cultures of murine tracheal epithelial cells.Nanotoxicology · 2020Article
- Toll-Like Receptor-Mediated Cardiac Injury during Experimental Sepsis.Mediators of inflammation · 2020Article
- Airway Epithelial Dynamics in Allergy and Related Chronic Inflammatory Airway Diseases.Frontiers in cell and developmental biology · 2020Review
- Acidosis potentiates endothelium-dependent vasorelaxation and gap junction communication in the superior mesenteric artery.European journal of pharmacology · 2018Article
- Connexin Communication Compartments and Wound Repair in Epithelial Tissue.International journal of molecular sciences · 2018Review
- Gap Junctions Are Involved in the Rescue of CFTR-Dependent Chloride Efflux by Amniotic Mesenchymal Stem Cells in Coculture with Cystic Fibrosis CFBE41o- Cells.Stem cells international · 2018Article
- MicroRNAs in mucosal inflammation.Journal of molecular medicine (Berlin, Germany) · 2017Review
- Secondhand Smoke-Prevalent Polycyclic Aromatic Hydrocarbon Binary Mixture-Induced Specific Mitogenic and Pro-inflammatory Cell Signaling Events in Lung Epithelial Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- What roles do colon stem cells and gap junctions play in the left and right location of origin of colorectal cancers?Journal of cell communication and signaling · 2017Article
- Outrunning the Red Queen: bystander activation as a means of outpacing innate immune subversion by intracellular pathogens.Cellular & molecular immunology · 2017Review
- Mind the Gaps in Tumor Immunity: Impact of Connexin-Mediated Intercellular Connections.Frontiers in immunology · 2017Review
- Autonomous immunity in mucosal epithelial cells: fortifying the barrier against infection.Microbes and infection · 2016Review
- Connexins, Pannexins, and Their Channels in Fibroproliferative Diseases.The Journal of membrane biology · 2016Review
- Suppression of Toll-like receptor-mediated innate immune responses at the ocular surface by the membrane-associated mucins MUC1 and MUC16.Mucosal immunology · 2015Article
- Junctional abnormalities in human airway epithelial cells expressing F508del CFTR.American journal of physiology. Lung cellular and molecular physiology · 2015Article
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 at 1 institution in 1 country.
Funding
Abstract
The innate immune response to inhaled bacteria, such as the opportunist Pseudomonas aeruginosa, is initiated by TLR2 displayed on the apical surface of airway epithelial cells. Activation of TLR2 is accompanied by an immediate Ca(2+) flux that is both necessary and sufficient to stimulate NF-kappaB and MAPK proinflammatory signaling to recruit and activate polymorphonuclear leukocytes in the airway. In human airway cells, gap junction channels were found to provide a regulated conduit for the movement of Ca(2+) from cell to cell. In response to TLR2 stimulation, by either lipid agonists or P. aeruginosa, gap junctions functioned to transiently amplify proinflammatory signaling by communicating Ca(2+) fluxes from stimulated to adjacent, nonstimulated cells thus increasing epithelial CXCL8 production. P. aeruginosa stimulation also induced tyrosine phosphorylation of connexin 43 and association with c-Src, events linked to the closure of these channels. By 4 h postbacterial stimulation, gap junction communication was decreased indicating an autoregulatory control of the connexins. Thus, gap junction channels comprised of connexin 43 and other connexins in airway cells provide a mechanism to coordinate and regulate the epithelial immune response even in the absence of signals from the immune system.
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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.