ArticlePLoS pathogens2016
Nitric Oxide Protects against Infection-Induced Neuroinflammation by Preserving the Stability of the Blood-Brain Barrier.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Sphenopalatine ganglion stimulation: a comprehensive evaluation across diseases in randomized controlled trials.Frontiers in neurology · 2024Pooled it
- Spent Hop (Cells · 2025Article
- Evaluation of salivary nitric oxide levels and anxiety in multiple sclerosis patients, with and without Xerostomia: correlation with clinical variables.BMC oral health · 2025Observational
- A Network Pharmacology Study and Experimental Validation to Identify the Potential Mechanism of Heparan Sulfate on Alzheimer's Disease-Related Neuroinflammation.Biomedicines · 2025Article
- Intraperitoneal Injection of theInternational journal of molecular sciences · 2024Article
- Treadmill running on neuropathic pain: via modulation of neuroinflammation.Frontiers in molecular neuroscience · 2024Review
- Article
- Argininosuccinate lyase deficiency causes blood-brain barrier disruption via nitric oxide-mediated dysregulation of claudin expression.JCI insight · 2023Article
- LMP2 deficiency causes abnormal metabolism, oxidative stress, neuroinflammation, myelin loss and neurobehavioral dysfunctions.Journal of translational medicine · 2023Article
- Article
- Nitric oxide in parasitic infections: a friend or foe?Journal of parasitic diseases : official organ of the Indian Society for Parasitology · 2022Review
- The Neuroprotection of Verbascoside in Alzheimer's Disease Mediated through Mitigation of Neuroinflammation via Blocking NF-κB-p65 Signaling.Nutrients · 2022Article
- Neuroimmunology of Common Parasitic Infections in Africa.Frontiers in immunology · 2022Review
- A mink (Neovison vison) model of self-injury: Effects of CBP-CREB axis on neuronal damage and behavior.Frontiers in veterinary science · 2022Article
- Nitric oxide modulation in neuroinflammation and the role of mesenchymal stem cells.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Erythrocytes, a New Contributor to Age-Associated Loss of Blood-Brain Barrier Integrity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Role of T cells during the cerebral infection with Trypanosoma brucei.PLoS neglected tropical diseases · 2021Article
- Proteomic and transcriptional changes associated with MeCP2 dysfunction reveal nodes for therapeutic intervention in Rett syndrome.Neurochemistry international · 2021Review
- Role of the inhibitor of serine peptidase 2 (ISP2) of Trypanosoma brucei rhodesiense in parasite virulence and modulation of the inflammatory responses of the host.PLoS neglected tropical diseases · 2021Article
- Association between Genetic Variants inViruses · 2021Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (NO) generated by inducible NO synthase (iNOS) is critical for defense against intracellular pathogens but may mediate inflammatory tissue damage. To elucidate the role of iNOS in neuroinflammation, infections with encephalitogenic Trypanosoma brucei parasites were compared in inos(-/-) and wild-type mice. Inos(-/-) mice showed enhanced brain invasion by parasites and T cells, and elevated protein permeability of cerebral vessels, but similar parasitemia levels. Trypanosome infection stimulated T cell- and TNF-mediated iNOS expression in perivascular macrophages. NO nitrosylated and inactivated pro-inflammatory molecules such as NF-κΒp65, and reduced TNF expression and signalling. iNOS-derived NO hampered both TNF- and T cell-mediated parasite brain invasion. In inos(-/-) mice, TNF stimulated MMP, including MMP9 activity that increased cerebral vessel permeability. Thus, iNOS-generated NO by perivascular macrophages, strategically located at sites of leukocyte brain penetration, can serve as a negative feed-back regulator that prevents unlimited influx of inflammatory cells by restoring the integrity of the blood-brain barrier.
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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.