ArticleParasites & vectors2014
The pathogenesis of optic neuritis caused by Angiostrongylus cantonensis in BALB/c mice.
Article in Parasites & vectors, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 13 citations in OpenAlex.
- IL-17A Mediates Demyelination by Activating A1 AstrocytesFrontiers in immunology · 2022Article
- Tanshinone IIA attenuates demyelination and promotes remyelination inInternational journal of biological sciences · 2019Article
- The opposite roles of PAS-5 and Galectin-1 in immune response during the early infection of Angiostrongylus cantonensis.Parasites & vectors · 2018Article
- Spleen atrophy related immune system changes attributed to infection of Angiostrongylus cantonensis in mouse model.Parasitology research · 2017Article
- Inhibiting Interleukin 17 Can Ameliorate the Demyelination Caused byMediators of inflammation · 2017Article
- Effects of albendazole combined with TSII-A (a Chinese herb compound) on optic neuritis caused by Angiostrongylus cantonensis in BALB/c mice.Parasites & vectors · 2015Article
- Preliminary expression profile of cytokines in brain tissue of BALB/c mice with Angiostrongylus cantonensis infection.Parasites & vectors · 2015Article
- Optic Neuritis: A Model for the Immuno-pathogenesis of Central Nervous System Inflammatory Demyelinating Diseases.Current immunology reviews · 2015Article
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9 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundOne of the most common causes of meningitis in South East Asia is angiostrongyliasis or infection by the parasitic nematode Angiostrongyliasis cantonensis. Although this nematode usually resides in the pulmonary arteries of rats, its incidental occurence in other hosts such as humans can cause optic neuritis and lead to serious vision sequelae. Nevertheless, there are currently no systematic studies conducted in this area.
methodsIn order to study the pathogenesis of optic neuritis, mice were tried as a new animal model to study and challenge with A. cantonensis on 7d, 14d and 21d, respectively. Electroretinogram (ERG), visual evoked potential (VEP), ophthalmoscopy and histology were examined on day 7d, 14d and 21d and tribendimidine (TBD) was later used to treat optic neuritis on day 14d for a week to evaluate its therapeutic effects.
resultsInfection of A. cantonensis caused obvious inflammatory cell infiltration in the retina and optic nerve adventitia in day 14d and 21d followed by optic nerve fiber demyelination and retinal ganglion swelling at day 21d in the challenged mice. Prolonged VEP latency and decreased ERG amplitude were also observed on day 21. After treatment of TBD in the infected mice, retinal and optic nerve inflammation were alleviated, but VEP latency and ERG amplitude did not improve on day 21d and 28d.
conclusionsThe current study provides evidence that A. cantonensis can cause optic neuritis along with optic nerve demyelination and retinal ganglion cell damage in a mouse model. TBD alone treatment can improve the symptoms of optic neuritis, but does not aid in vision recovery, suggesting that both neuroprotective agents and Dexamethasone should be administered, along with treatment for the infection, to protect the optic nerve and ganglion cells. Furthermore, as the symptoms of optic neuritis caused by A. cantonensis in mice are similar to the optic neuritis in multiple sclerosis (MS) human patients, we suggest that the BALB/c mouse model provided in this study may be useful to explore therapies of optic neuritis in MS patients.
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