ArticlePloS one2013
Prevention of LPS-induced microglia activation, cytokine production and sickness behavior with TLR4 receptor interfering peptides.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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
82 citing papers in PubMed, 168 citations in OpenAlex.
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- Gut-Brain Inflammation and Disrupted Homeostasis Due to Activation of Mast Cells and Microglia.International journal of molecular sciences · 2026Review
- Pyridostigmine Attenuated Placental Ischemia-Upregulated Paraventricular Nucleus TLR4-Associated Hypertension in Preeclamptic Rats.Molecular neurobiology · 2026Article
- Inflammation increases the penetrance of behavioral impairment inbioRxiv : the preprint server for biology · 2025Article
- Metabolic Flexibility of Microglia: Energy Substrate Utilization and Impact on Neuronal Metabolism.Journal of neurochemistry · 2025Article
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- In Vitro Antioxidant and Anti-Neuroinflammatory Effects ofLife (Basel, Switzerland) · 2025Article
- VPAC1 and VPAC2 Receptor Heterozygosity Confers Distinct Biological Properties to BV2 Microglial Cells.Cells · 2025Article
- Exercise, Diet, and Brain Health: From the Perspective of Gut Microbiota Regulation.Nutrients · 2025Review
- Innate Immune Mechanisms in the Central Nervous System.Advances in experimental medicine and biology · 2025Review
- Adolescent morphine exposure does not alter low-dose lipopolysaccharide (LPS)-induced sickness behavior in adult C57/BL6 mice.PloS one · 2025Article
- In Vitro Analysis of LPS-Induced miRNA Differences in Bovine Endometrial Cells and Study of Related Pathways.Animals : an open access journal from MDPI · 2024Article
- Constitutive expression of the deubiquitinating enzyme CYLD does not affect microglia phenotype or function in homeostasis and neuroinflammation.Journal of molecular medicine (Berlin, Germany) · 2024Article
- Toward discovering a novel family of peptides targeting neuroinflammatory states of brain microglia and astrocytes.Journal of neurochemistry · 2024Article
- Physcion Mitigates LPS-Induced Neuroinflammation, Oxidative Stress, and Memory Impairments via TLR-4/NF-кB Signaling in Adult Mice.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Exosomes secreted from induced pluripotent stem cell ameliorate the lipopolysaccharide induced neuroinflammatory response via lncRNA-0949.Immunity, inflammation and disease · 2024Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The innate immune receptor Toll-like 4 (TLR4) is the receptor activated by lipopolysaccharide (LPS), and TLR4-LPS interaction is well known to induce an innate immune response, triggering sickness behavior. Within the brain, TLR4 is highly expressed in brain microglia, and excessive inflammation resulting from activation of this pathway in the brain has been implicated in depressive disorders and neurodegenerative pathologies. We hypothesized that blocking LPS-induced activation of TLR4 would prevent downstream immune signaling in the brain and suppress the induction of sickness behavior. We used interfering peptides to block TLR4 activation and confirmed their efficacy in preventing second messenger activation and cytokine production normally induced by LPS treatment. Further, these peptides blocked morphological changes in microglia that are typically induced by LPS. We also demonstrated that intraperitoneal (i.p.) injection of Tat-TLR4 interfering peptides prevented LPS-induced sickness behavior, as assessed in home cage behavior and with the intracranial self-stimulation paradigm. These newly synthesised peptides inhibit TLR4 signaling thereby preventing changes in behavior and motivation caused by inflammatory stimuli. These peptides highlight the roll of TLR4 and microglia morphology changes in sickness behavior, and thus may be of therapeutic value in limiting the deleterious impact of excessive inflammation in specific CNS pathologies.
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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.