ArticleJournal of cellular and molecular medicine2019
CXCL16/CXCR6 is involved in LPS-induced acute lung injury via P38 signalling.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- Trial
- Redox-regulated in situ-forming hydrogel informed by single-cell transcriptomics for functional restoration of injured vocal folds.Nature communications · 2026Article
- Article
- Advancements in understanding and treating CXCL16/CXCR6 in tumors and in inflammatory diseases: a narrative review.Frontiers in immunology · 2026Review
- Single-cell transcriptomics identifies altered neutrophil dynamics and accentuated T-cell cytotoxicity in tobacco flavored e-cigarette exposed mouse lungs.bioRxiv : the preprint server for biology · 2025Article
- Protective Effect of Low 2-O, 3-O Desulfated Heparin (ODSH) Against LPS-Induced Acute Lung Injury in Mice.Biomolecules · 2025Article
- Cold ischemia time alters cell-type specific senescence leading to loss of cellular integrity in mouse lungs.Experimental lung research · 2024Article
- Pien Tze Huang alleviates Concanavalin A-induced autoimmune hepatitis by regulating intestinal microbiota and memory regulatory T cells.World journal of gastroenterology · 2023Article
- Evaluating Novel Protein Phosphatase 2A Activators as Therapeutics for Emphysema.American journal of respiratory cell and molecular biology · 2023Article
- sCXCL16 as a prognostic biomarker for COVID-19 outcome.Journal of medical virology · 2023Article
- The main e-cigarette component vegetable glycerin enhances neutrophil migration and fibrosis in endotoxin-induced lung injury via p38 MAPK activation.Respiratory research · 2023Article
- Review
- Exosomes derived from dental pulp stem cells accelerate cutaneous wound healing by enhancing angiogenesis via the Cdc42/p38 MAPK pathway.International journal of molecular medicine · 2022Article
- Poldip2 knockdown protects against lipopolysaccharide-induced acute lung injuryFrontiers in pharmacology · 2022Article
- CCL25 Inhibition Alleviates Sepsis-Induced Acute Lung Injury and Inflammation.Infection and drug resistance · 2022Article
- The Host-Microbiome Response to Hyperbaric Oxygen Therapy in Ulcerative Colitis Patients.Cellular and molecular gastroenterology and hepatology · 2022Article
- Further comment on articles pertaining to: "Homocysteine as a potential predictor of cardiovascular risk in patients with COVID-19".Medical hypotheses · 2021Article
- The α2AR/Caveolin-1/p38MAPK/NF-κB axis explains dexmedetomidine protection against lung injury following intestinal ischaemia-reperfusion.Journal of cellular and molecular medicine · 2021Article
- Genetic and epigenetic factors associated with increased severity of Covid-19.Cell biology international · 2021Review
- The Emerging Roles of Tripartite Motif Proteins (TRIMs) in Acute Lung Injury.Journal of immunology research · 2021Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although several chemokines play key roles in the pathogenesis of acute lung injury (ALI), the roles of chemokine (C-X-C motif) ligand 16 (CXCL16) and its receptor C-X-C chemokine receptor type 6 (CXCR6) in ALI pathogenesis remain to be elucidated. The mRNA and protein expression of CXCL16 and CXCR6 was detected after lipopolysaccharide (LPS) stimulation with or without treatment with the nuclear factor-κB (NF-κB) inhibitor pyrrolidine dithiocarbamate (PDTC). Lung injury induced by LPS was evaluated in CXCR6 knockout mice. CXCL16 level was elevated in the serum of ALI patients (n = 20) compared with healthy controls (n = 30). CXCL16 treatment (50, 100, and 200 ng/mL) in 16HBE cells significantly decreased the epithelial barrier integrity and E-cadherin expression, and increased CXCR6 expression, reactive oxygen species (ROS) production, and p38 phosphorylation. Knockdown of CXCR6 or treatment with the p38 inhibitor SB203580 abolished the effects of CXCL16. Moreover, treatment of 16HBE cells with LPS (5, 10, 20 and 50 μg/mL) significantly increased CXCL16 release as well as the mRNA and protein levels of CXCL16 and CXCR6. The effects of LPS treatment (20 μg/mL) were abolished by treatment with PDTC. The results of the luciferase assay further demonstrated that PDTC treatment markedly inhibited the activity of the CXCL16 promoter. In conclusion, CXCL16, whose transcription was enhanced by LPS, may be involved in ROS production, epithelial barrier dysfunction and E-cadherin down-regulation via p38 signalling, thus contributing to the pathogenesis of ALI. Importantly, CXCR6 knockout or inhibition of p38 signalling may protect mice from LPS-induced lung injury by decreasing E-cadherin expression.
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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.