ArticleJournal of neuroinflammation2020
Microglia depletion fails to abrogate inflammation-induced sickness in mice and rats.
Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 75 citations in OpenAlex.
- Where's my mom? Resilient maternal preference in post-weaning male and female mice within a multi-chamber social behavior task.Brain, behavior, & immunity - health · 2025Article
- Neuroimmune crosstalk in chronic neuroinflammation: microglial interactions and immune modulation.Frontiers in cellular neuroscience · 2025Review
- Microglia in the aged brain develop a hypoactive molecular phenotype after surgery.Journal of neuroinflammation · 2024Article
- Microglia drive diurnal variation in susceptibility to inflammatory blood-brain barrier breakdown.JCI insight · 2024Article
- The role of microglia in 67NR mammary tumor-induced suppression of brain responses to immune challenges in female mice.Journal of neurochemistry · 2024Article
- Novel microglial transcriptional signatures promote social and cognitive deficits following repeated social defeat.Communications biology · 2024Article
- Repeated LPS induces training and tolerance of microglial responses across brain regions.Journal of neuroinflammation · 2024Article
- Microglia contribute to mammary tumor-induced neuroinflammation in a female mouse model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Pan-Cancer Analysis Reveals Disulfidoptosis-Associated Genes as Promising Immunotherapeutic Targets: Insights Gained from Bulk Omics and Single-Cell Sequencing Validation.Biomedicines · 2024Article
- T Cell-Induced Colitis Is Exacerbated by Prolonged Stress: A Comparison in Male and Female Mice.Biomedicines · 2024Article
- Immune mechanisms of depression in rheumatoid arthritis.Nature reviews. Rheumatology · 2023Review
- Cytokine enrichment in deep cerebellar nuclei is contributed by multiple glial populations and linked to reduced amyloid plaque pathology.Journal of neuroinflammation · 2023Article
- The role of molecular chaperones in the mechanisms of epileptogenesis.Cell stress & chaperones · 2023Review
- Distinguishing the effects of systemic CSF1R inhibition by PLX3397 on microglia and peripheral immune cells.Journal of neuroinflammation · 2023Article
- Depletion of microglia with PLX3397 attenuates MK-801-induced hyperactivity associated with regulating inflammation-related genes in the brain.Zoological research · 2023Article
- Review
- Partial Depletion of Microglia Attenuates Long-Term Potentiation Deficits following Repeated Blast Traumatic Brain Injury in Organotypic Hippocampal Slice Cultures.Journal of neurotrauma · 2023Article
- Macrophage regulation of the "second brain": CD163 intestinal macrophages interact with inhibitory interneurons to regulate colonic motility - evidence from theFrontiers in immunology · 2023Article
- Limitations of PLX3397 as a microglial investigational tool: peripheral and off-target effects dictate the response to inflammation.Frontiers in immunology · 2023Article
- Evolutionary Aspects of Infections: Inflammation and Sickness Behaviors.Current topics in behavioral neurosciences · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundProduction of inflammatory mediators by reactive microglial cells in the brain is generally considered the primary mechanism underlying the development of symptoms of sickness in response to systemic inflammation.
methodsDepletion of microglia was achieved in C57BL/6 mice by chronic oral administration of PLX5622, a specific antagonist of colony stimulating factor-1 receptor, and in rats by a knock-in model in which the diphtheria toxin receptor was expressed under the control of the endogenous fractalkine receptor (CX3CR1) promoter sequence. After successful microglia depletion, mice and rats were injected with a sickness-inducing dose of lipopolysaccharide according to a 2 (depletion vs. control) × 2 (LPS vs. saline) factorial design. Sickness was measured by body weight loss and decreased locomotor activity in rats and mice, and reduced voluntary wheel running in mice.
resultsChronic administration of PLX5622 in mice and administration of diphtheria toxin to knock-in rats depleted microglia and peripheral tissue macrophages. However, it did not abrogate the inducible expression of proinflammatory cytokines in the brain in response to LPS and even exacerbated it for some of the cytokines. In accordance with these neuroimmune effects, LPS-induced sickness was not abrogated, rather it was exacerbated when measured by running wheel activity in mice.
conclusionsThese findings reveal that the sickness-inducing effects of acute inflammation can develop independently of microglia activation.
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