ArticleParasitology research2012
Differences of larval development and pathological changes in permissive and nonpermissive rodent hosts for Angiostrongylus cantonensis infection.
Article in Parasitology research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 46 citations in OpenAlex.
- AcNR1F orchestrates epidermal remodeling to enable host adaptation in Angiostrongylus cantonensis.PLoS pathogens · 2026Article
- Isolate-specific rat brain transcriptional responses to rat lungworm (Angiostrongylus cantonensis).Pathogens and disease · 2025Article
- Inflammatory and immunopathological differences in brains of permissive and non-permissive hosts with Angiostrongylus cantonensis infection can be identified using 18F/FDG/PET-imaging.PLoS neglected tropical diseases · 2024Article
- Mechanisms of the host immune response and helminth-induced pathology during Trichobilharzia regenti (Schistosomatidae) neuroinvasion in mice.PLoS pathogens · 2022Article
- Interleukin 17A Derived from γδ T Cell Induces Demyelination of the Brain in Angiostrongylus cantonensis Infection.Molecular neurobiology · 2021Article
- Newly developed SYBR Green-based quantitative real-time PCRs revealed coinfection evidence ofFood and waterborne parasitology · 2021Article
- Co-Therapy of Albendazole and Dexamethasone Reduces Pathological Changes in the Cerebral Parenchyma of Th-1 and Th-2 Dominant Mice Heavily Infected withBiomolecules · 2021Article
- CXFrontiers in cellular and infection microbiology · 2021Article
- Albendazole-Schisandrin B Co-Therapy onBiomolecules · 2020Article
- Magnetic resonance imaging findings and clinical manifestations in cerebral angiostrongyliasis from Dali, China.Brain and behavior · 2019Article
- Necroptosis andFrontiers in microbiology · 2019Article
- Trichostatin A, a Histone Deacetylase Inhibitor, Alleviates Eosinophilic Meningitis Induced byFrontiers in microbiology · 2019Article
- Apoptosis and necroptosis of mouse hippocampal and parenchymal astrocytes, microglia and neurons caused by Angiostrongylus cantonensis infection.Parasites & vectors · 2017Article
- Soluble antigens from the neurotropic pathogen Angiostrongylus cantonensis directly induce thymus atrophy in a mouse model.Oncotarget · 2017Article
- Neuronal Apoptosis: Pathological Basis of Behavioral Dysfunctions Induced byThe Korean journal of parasitology · 2017Article
- Spleen atrophy related immune system changes attributed to infection of Angiostrongylus cantonensis in mouse model.Parasitology research · 2017Article
- Activation of the hypothalamic-pituitary-adrenal (HPA) axis contributes to the immunosuppression of mice infected with Angiostrongylus cantonensis.Journal of neuroinflammation · 2016Article
- Cysticercus fasciolaris infection induced oxidative stress and apoptosis in rat liver: a strategy for host-parasite cross talk.Parasitology research · 2016Article
- Preliminary expression profile of cytokines in brain tissue of BALB/c mice with Angiostrongylus cantonensis infection.Parasites & vectors · 2015Article
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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
Angiostrongylus cantonensis is a neurotrophic and pulmonary parasite which causes severe neuropathological damages by invading and developing in the central nervous system (CNS). Nonpermissive host with A. cantonensis infection appeared to have more serious neurologic symptoms, and there is still not much knowledge about the host-parasite interrelationship in different hosts. We investigated and compared the larval size, recovery rate, distribution, and the severity of pathologic injuries in the CNS of both permissive host (e.g., rats) and nonpermissive hosts (e.g., mice). In present study, mice infected with A. cantonensis showed higher worm recovery rate in late-stage infection and smaller size of intracranial larvae as compared to the infected rats. Intracranial larvae mainly aggregated on cerebral surface of infected rats but on surface of cerebellum and brainstem in mice. Hemorrhage and tissue edema on brain surface caused by worm migration appeared earlier and severer in infected mice than in rats. Neuropathological examination revealed that injuries induced by A. cantonensis in brain parenchyma included hemorrhage, vascular dilatation, focal necrosis with neuronal loss, and infiltration of inflammatory cells. In the comparison of these pathological changes in rats and mice, infected mice suffered more serious injuries and provoked more intense inflammatory response as compared to infected rats. All these morphological evidences indicate that larval development was retardant in the CNS of nonpermissive host, and nonpermissive host experienced more serious pathological injuries than permissive host. It implies that the difference in innate immune response to parasite infection attribute to host specificity.
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