ArticlePLoS pathogens2025
Astrocyte-derived complement C3 facilitated microglial phagocytosis of synapses in Staphylococcus aureus-associated neurocognitive deficits.
Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Loss of C3 and CD14 reduces region-specific neuroinflammation in a murine polytrauma model.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- hUC-MSCs transplantation promotes neurological recovery by ameliorating spinal cord injury and hippocampal synaptic remodeling in female mice.Journal of orthopaedic translation · 2026Article
- Neuropsychiatric disorders in pulmonary fibrosis: from brain network alterations to inflammatory mechanisms and therapeutic implications.Journal of neuroinflammation · 2026Review
- Review
- Panacis Quinquefolii Radix Polysaccharides Alleviate Depressive-Like Behaviors in Chronic Unpredictable Mild Stress-Induced Mice by Suppressing Complement C1Q/C3-Mediated Microglial Synaptic Pruning and Modulating Gut Microbiota.CNS neuroscience & therapeutics · 2026Article
- Innate Immune Evasion of Lyme Disease Pathogen Drives Alzheimer-Like Pathology.Research square · 2026Article
- Spatial omics of neuroinflammation: insights across brain diseases.Frontiers in immunology · 2026Review
- Molecular signaling pathways shaping astrocyte-microglia crosstalk in health and disease.Frontiers in molecular neuroscience · 2026Review
- Systemic Neurodegeneration and Brain Aging: Multi-Omics Disintegration, Proteostatic Collapse, and Network Failure Across the CNS.Biomedicines · 2025Review
- Increased Synapse Elimination by Inflammatory Cells Contributes to Long-lasting Post-Stroke Memory Dysfunction in Old Mice.bioRxiv : the preprint server for biology · 2025Article
- Glial-mediated immune modulation in glaucomatous neurodegeneration: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
The presence of pathogens is a significant challenge in causing brain infections and tissue damage. There is growing evidence that pathogen infections are commonly associated with cognitive dysfunction and mental health problems, but the underlying mechanisms are not yet fully understood. Here, we found microglia and astrocyte activation, neuronal damage, synapse loss, and cognitive impairment in a Staphylococcus aureus (S. aureus) induced mouse model. An unbiased transcription profile of isolated microglia derived from S. aureus-infected mice identified the involvement of microglial phagosome and regulation of neurogenesis. Our findings indicate that the complement C1q and C3 are upregulated, and astroglial release of C3 activates microglia to phagocytose synapses. Blocking the C3-C3aR axis can improve microglial phagocytosis, thus rescuing synapse loss and cognitive impairment in infected mice. These results indicate that S. aureus induces synapse elimination and cognitive impairment by activating microglia and astrocytes through C3-C3aR signaling. This suggests a mechanism of complement signaling bridged crosstalk between astrocyte and microglia in the S. aureus-associated post-infectious synapse loss and cognitive dysfunction, and provide potential therapeutic targets for managing pathogen-associated brain infections.
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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.