ArticleThe American journal of pathology2005
Toxoplasma gondii prevents neuron degeneration by interferon-gamma-activated microglia in a mechanism involving inhibition of inducible nitric oxide synthase and transforming growth factor-beta1 production by infected microglia.
Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Association between Toxoplasma gondii Infection and Risk of Parkinson's Disease: A Systematic Review and Meta-Analysis.BioMed research international · 2019Pooled it
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- Pathological mechanisms of glial cell activation and neurodegenerative and neuropsychiatric disorders caused byFrontiers in microbiology · 2024Review
- Alzheimer's disease and infectious agents: a comprehensive review of pathogenic mechanisms and microRNA roles.Frontiers in neuroscience · 2024Review
- Chronic infection by atypicalBrain, behavior, & immunity - health · 2023Article
- Toxoplasmosis: Targeting neurotransmitter systems in psychiatric disorders.Metabolic brain disease · 2022Review
- Epidemiology, Pathophysiology, Diagnosis, and Management of Cerebral Toxoplasmosis.Clinical microbiology reviews · 2021Review
- Influence of the Host and Parasite Strain on the Immune Response DuringFrontiers in cellular and infection microbiology · 2020Review
- ROP18-Mediated Transcriptional Reprogramming of HEK293T Cell Reveals New Roles of ROP18 in the Interplay BetweenFrontiers in cellular and infection microbiology · 2020Article
- Sero-prevalence of Toxoplasma gondii and associated risk factors among psychiatric outpatients attending University of Gondar Hospital, Northwest Ethiopia.BMC infectious diseases · 2019Article
- Chronic Toxoplasma infection is associated with distinct alterations in the synaptic protein composition.Journal of neuroinflammation · 2018Article
- Cofilin Mediates LPS-Induced Microglial Cell Activation and Associated Neurotoxicity Through Activation of NF-κB and JAK-STAT Pathway.Molecular neurobiology · 2018Article
- Characteristics of Infection Immunity Regulated byFrontiers in immunology · 2018Article
- Host-Frontiers in immunology · 2017Review
- Nitric oxide and cytokine production by glial cells exposed in vitro to neuropathogenic schistosome Trichobilharzia regenti.Parasites & vectors · 2016Article
- The known and missing links between Toxoplasma gondii and schizophrenia.Metabolic brain disease · 2016Review
- Chronic Toxoplasma gondii infection enhances β-amyloid phagocytosis and clearance by recruited monocytes.Acta neuropathologica communications · 2016Article
- Protective immunity against acute toxoplasmosis in BALB/c mice induced by a DNA vaccine encoding Toxoplasma gondii elongation factor 1-alpha.BMC infectious diseases · 2015Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interferon (IFN)-gamma, the main cytokine responsible for immunological defense against Toxoplasma gondii, is essential in all infected tissues, including the central nervous system. However, IFN-gamma-activated microglia may cause tissue injury through production of toxic metabolites such as nitric oxide (NO), a potent inducer of central nervous system pathologies related to inflammatory neuronal disturbances. Despite potential NO toxicity, neurodegeneration is not commonly found during chronic T. gondii infection. In this study, we describe decreased NO production by IFN-gamma-activated microglial cells infected by T. gondii. This effect involved strong inhibition of iNOS expression in IFN-gamma-activated, infected microglia but not in uninfected neighboring cells. The inhibition of NO production and iNOS expression were parallel with recovery of neurite outgrowth when neurons were co-cultured with T. gondii-infected, IFN-gamma-activated microglia. In the presence of transforming growth factor (TGF)-beta1-neutralizing antibodies, the beneficial effect of the parasite on neurons was abrogated, and NO production reverted to levels similar to IFN-gamma-activated uninfected co-cultures. In addition, we observed Smad-2 nuclear translocation, a hallmark of TGF-beta1 downstream signaling, in infected microglial cultures, emphasizing an autocrine effect restricted to infected cells. Together, these data may explain a neuropreservation pattern observed during immunocompetent host infection that is dependent on T. gondii-triggered TGF-beta1 secretion by infected microglia.
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