ArticleJournal of molecular neuroscience : MN2014
AChE and RACK1 promote the anti-inflammatory properties of fluoxetine.
Article in Journal of molecular neuroscience : MN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Effects of psychotropic drugs on inflammation: consequence or mediator of therapeutic effects in psychiatric treatment?Psychopharmacology · 2016Pooled it
- Integrative Analysis of Drug Co-Prescriptions in Peritoneal Dialysis Reveals Molecular Targets and Novel Strategies for Intervention.Journal of clinical medicine · 2025Article
- The roles of RACK1 in the pathogenesis of Alzheimer's disease.Journal of biomedical research · 2024Article
- Inhibitory effects of fluoxetine on the secretion of inflammatory mediators and JAK/STAT3 and JNK/TLR4 gene expression.Molecular biology reports · 2023Article
- Targeting neurotransmitter-mediated inflammatory mechanisms of psychiatric drugs to mitigate the double burden of multimorbidity and polypharmacy.Brain, behavior, & immunity - health · 2021Article
- Suppression of cigarette smoke induced MMP1 expression by selective serotonin re-uptake inhibitors.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Involvement of proBDNF in Monocytes/Macrophages with Gastrointestinal Disorders in Depressive Mice.Neurotoxicity research · 2020Article
- Interacting withActa pharmaceutica Sinica. B · 2020Article
- Fluoxetine attenuates neuroinflammation in early brain injury after subarachnoid hemorrhage: a possible role for the regulation of TLR4/MyD88/NF-κB signaling pathway.Journal of neuroinflammation · 2018Article
- Differential Peripheral Proteomic Biosignature of Fluoxetine Response in a Mouse Model of Anxiety/Depression.Frontiers in cellular neuroscience · 2017Article
- Intestinal Serotonin Transporter Inhibition by Toll-Like Receptor 2 Activation. A Feedback Modulation.PloS one · 2016Article
- Gut feeling: MicroRNA discriminators of the intestinal TLR9-cholinergic links.International immunopharmacology · 2015Article
- Role of acetylcholinesterase in lung cancer.Thoracic cancer · 2015Review
- Chronic morphine-induced microRNA-124 promotes microglial immunosuppression by modulating P65 and TRAF6.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Valproic acid potentiates curcumin-mediated neuroprotection in lipopolysaccharide induced rats.Frontiers in cellular neuroscience · 2014Article
- Upregulating nonneuronal cholinergic activity decreases TNF release from lipopolysaccharide-stimulated RAW264.7 cells.Mediators of inflammation · 2014Article
- Systemic effects of fluoxetine on the amount of tooth movement, root resorption, and alveolar bone remodeling during orthodontic force application in rat.Dental research journalArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Selective serotonin reuptake inhibitors (SSRIs) show anti-inflammatory effects, suggesting a possible interaction with both Toll-like-receptor 4 (TLR4) responses and cholinergic signaling through as yet unclear molecular mechanism(s). Our results of structural modeling support the concept that the antidepressant fluoxetine physically interacts with the TLR4-myeloid differentiation factor-2 complex at the same site as bacterial lipopolysaccharide (LPS). We also demonstrate reduced LPS-induced pro-inflammatory interleukin-6 and tumor necrosis factor alpha in human peripheral blood mononuclear cells preincubated with fluoxetine. Furthermore, we show that fluoxetine intercepts the LPS-induced decreases in intracellular acetylcholinesterase (AChE-S) and that AChE-S interacts with the nuclear factor kappa B (NFκB)-activating intracellular receptor for activated C kinase 1 (RACK1). This interaction may prevent NFκB activation by residual RACK1 and its interacting protein kinase PKCβII. Our findings attribute the anti-inflammatory properties of SSRI to surface membrane interference with leukocyte TLR4 activation accompanied by intracellular limitation of pathogen-inducible changes in AChE-S, RACK1, and PKCβII.
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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.