ArticleImmunology2008
Toll-like receptor agonists stimulate human neutrophil migration via activation of mitogen-activated protein kinases.
Article in Immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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
29 citing papers in PubMed, 58 citations in OpenAlex.
- Dual host and pathogen targeting by MEK1/2 inhibitors.Infection and immunity · 2026Review
- Bridging metabolic reprogramming and targeted therapy: the critical role of S-palmitoylation in cancer.Frontiers in cell and developmental biology · 2026Review
- Palmitoylation in cancer: decoding its roles in signal transduction, tumor immunity, and emerging therapeutic opportunities.Frontiers in immunology · 2025Review
- Impact of Selected Bacterial and Viral Toll-like Receptor Agonists on the Phenotype and Function of Camel Blood Neutrophils.Veterinary sciences · 2023Article
- Hyaluronan promotes intracellular ROS production and apoptosis in TNFα-stimulated neutrophils.Frontiers in immunology · 2023Article
- Regulation of TLR10 Expression and Its Role in Chemotaxis of Human Neutrophils.Journal of innate immunity · 2022Article
- Comparable bidirectional neutrophil immune dysregulation between Kawasaki disease and severe COVID-19.Frontiers in immunology · 2022Article
- VEGF receptor 2 (KDR) protects airways from mucus metaplasia through a Sox9-dependent pathway.Developmental cell · 2021Article
- Article
- Protective role of curcumin against lipopolysaccharide-induced inflammation and apoptosis in human neutrophil.Anesthesia and pain medicine · 2020Article
- The Expression of Glycoprotein Genes in the Inflammatory Process of Kawasaki Disease.Frontiers in pediatrics · 2020Article
- P-MAPA, a Fungi-Derived Immunomodulatory Compound, Induces a Proinflammatory Response in a Human Whole Blood Model.Mediators of inflammation · 2020Article
- Spz/Toll-6 signal guides organotropic metastasis inDisease models & mechanisms · 2019Article
- The Vitamin D Binding Protein and Inflammatory Injury: A Mediator or Sentinel of Tissue Damage?Frontiers in endocrinology · 2019Review
- Impact of toll-like receptor 4 stimulation on human neonatal neutrophil spontaneous migration, transcriptomics, and cytokine production.Journal of molecular medicine (Berlin, Germany) · 2018Article
- Multiple Phenotypic Changes Define Neutrophil Priming.Frontiers in cellular and infection microbiology · 2017Review
- Filifactor alocis Promotes Neutrophil Degranulation and Chemotactic Activity.Infection and immunity · 2016Article
- Systemic vasculitis associated with vemurafenib treatment: Case report and literature review.Medicine · 2016Review
- Tanreqing Injection Attenuates Lipopolysaccharide-Induced Airway Inflammation through MAPK/NF-κB Signaling Pathways in Rats Model.Evidence-based complementary and alternative medicine : eCAM · 2016Article
- Cell surface topography is a regulator of molecular interactions during chemokine-induced neutrophil spreading.Biophysical journal · 2014Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human neutrophil migratory responses to Toll-like receptor (TLR) agonists were studied using videomicroscopy. When challenged with lipopolysaccharide (LPS, TLR4 agonist) or N-palmitoyl-S-[2,3-bis(palmitoyloxy)-(2RS)-propyl]-(R)-cysteinyl-seryl-(lysyl)(3)-lysine (P3CSK4, TLR2 agonist), neutrophils displayed enhanced motility, which was found to reflect increased random migration but not directed migration (chemotaxis). Enhanced neutrophil motility was detected within 10 min after stimulation with LPS or P3CSK4, and was sustained for more than 80 min. Stimulation of neutrophils with LPS or P3CSK4 resulted in the activation of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK), which preceded neutrophil migration. TLR-mediated neutrophil migration was strongly suppressed by pretreatment of cells with U0126 (MAPK/ERK kinase inhibitor) but not with U0124 (an inactive analogue of U0126) or SB203580 (a p38 MAPK inhibitor), and was almost completely abolished by pretreatment of cells with U0126 and SB203580 in combination. Randomly migrating neutrophils in response to LPS or P3CSK4 displayed directed migration when further challenged with gradient concentrations of N-formyl-methionyl-leucyl-phenylalanine (FMLP) or platelet-activating factor (PAF). These findings indicate that TLR agonists stimulate human neutrophil migration via the activation of ERK and p38 MAPK, and FMLP- or PAF-induced neutrophil chemotaxis is not affected by the pre-exposure of cells to TLR agonists.
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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.