ArticleNeuroscience2009
The contributing role of CD14 in toll-like receptor 4 dependent neuropathic pain.
Article in Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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
56 citing papers in PubMed, 111 citations in OpenAlex.
- Analytical subcellular fractionation of microglial BV-2 cells with peroxisomal beta-oxidation defect.Histochemistry and cell biology · 2025Article
- The Causal Relationship Between Immune Cells and Neuropathic Pain: A Two-Sample Mendelian Randomization Study Based on Genome-Wide Association Analysis.Journal of pain research · 2025Article
- Neuroactive Steroids, Toll-like Receptors, and Neuroimmune Regulation: Insights into Their Impact on Neuropsychiatric Disorders.Life (Basel, Switzerland) · 2024Review
- Chondroitin sulfate proteoglycans prevent immune cell phenotypic conversion and inflammation resolution via TLR4 in rodent models of spinal cord injury.Nature communications · 2022Article
- Article
- Adipose Tissue Myeloid-Lineage Neuroimmune Cells Express Genes Important for Neural Plasticity and Regulate Adipose Innervation.Frontiers in endocrinology · 2022Article
- Toll-like receptor 4/nuclear factor-kappa B pathway is involved in radicular pain by encouraging spinal microglia activation and inflammatory response in a rat model of lumbar disc herniation.The Korean journal of pain · 2021Article
- Review
- Lipid rafts in glial cells: role in neuroinflammation and pain processing.Journal of lipid research · 2020Review
- Microglial activation and responses to vasculature that result from an acute LPS exposure.Neurotoxicology · 2020Article
- Inflammatory mediators of opioid tolerance: Implications for dependency and addiction.Peptides · 2019Review
- Neuraxial TNF and IFN-beta co-modulate persistent allodynia in arthritic mice.Brain, behavior, and immunity · 2019Article
- Electroacupuncture Alleviates Spared Nerve Injury-Induced Neuropathic Pain And Modulates HMGB1/NF-κB Signaling Pathway In The Spinal Cord.Journal of pain research · 2019Article
- Inhibition of Neuroinflammation by AIBP: Spinal Effects upon Facilitated Pain States.Cell reports · 2018Article
- Toll-like receptors and their role in persistent pain.Pharmacology & therapeutics · 2018Review
- TLR4-mediated autophagic impairment contributes to neuropathic pain in chronic constriction injury mice.Molecular brain · 2018Article
- Article
- TLR4 Signaling Pathway Modulators as Potential Therapeutics in Inflammation and Sepsis.Vaccines · 2017Review
- TLR4 antagonist FP7 inhibits LPS-induced cytokine production and glycolytic reprogramming in dendritic cells, and protects mice from lethal influenza infection.Scientific reports · 2017Article
- Effect of pioglitazone on neuropathic pain and spinal expression of TLR-4 and cytokines.Experimental and therapeutic medicine · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We have previously demonstrated that CNS toll-like receptor 4 (TLR4) plays a key role in the development of behavioral hypersensitivity in a rodent model of neuropathic pain, spinal nerve L5 transection (L5Tx). TLR4 is a well-known receptor for lipopolysaccharide (LPS) in innate immune responses. In the current study, we further investigated the role of CD14, an accessory molecule in the LPS-TLR4 signaling pathway, in the development of L5Tx-induced neuropathic pain. CD14 knockout (KO) mice displayed significantly decreased behavioral sensitivity (mechanical allodynia and thermal hyperalgesia) as early as day 1 post-L5Tx, indicating a nociceptive role of CD14. By flow cytometric analyses, we observed significantly elevated microglial surface CD14 expression in the ipsilateral lumbar spinal cord 3 days post-L5Tx, as well as remarkable increases in microglial size (via forward scatter (FSC)) and granularity (via side scatter (SSC)). Further, intrathecal injection of soluble CD14 induced significantly greater mechanical hypersensitivity in wild type (C3H/HeN) mice compared with TLR4-deficient (C3H/HeJ) mice. Together, these data demonstrate that CD14 plays a contributing role in TLR4-dependent nerve injury-induced neuropathic pain.
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.