ArticleParasites & vectors2017
Apoptosis and necroptosis of mouse hippocampal and parenchymal astrocytes, microglia and neurons caused by Angiostrongylus cantonensis infection.
Article in Parasites & vectors, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 57 citations in OpenAlex.
- Dynamic alterations and potential roles of gut microbiota and metabolites in Angiostrongylus cantonensis-infected mice and rats.Infectious diseases of poverty · 2026Article
- Albendazole-doxycycline combination therapy alleviates MRI- and pathology-evident neuroinflammation and restores IL-33/GFAP balance in mouse neuroangiostrongyliasis.Parasites & vectors · 2026Article
- Caspase-8 expression in CD8Science advances · 2025Article
- CX3CL1/CX3CR1 involved modulation of microglial activation and eosinophilic meningoencephalitis in angiostrongyliasis.Food and waterborne parasitology · 2025Article
- The Innate Immune Sensor Zbp1 Mediates Central Nervous System Inflammation Induced by Angiostrongylus Cantonensis by Promoting Macrophage Inflammatory Phenotypes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Exploration of the Molecular Mechanism by Which Caveolin-1 Regulates Changes in Blood-Brain Barrier Permeability Leading to Eosinophilic Meningoencephalitis.Tropical medicine and infectious disease · 2024Article
- Angiostrongylus cantonensis induces energy imbalance and dyskinesia in mice by reducing the expression of melanin-concentrating hormone.Parasites & vectors · 2024Article
- Efficacy of artemether against toxocariasis in mice: parasitological and immunopathological changes in brain, liver, and lung.Pathogens and global health · 2024Article
- Different phenotypes of microglia in animal models of Alzheimer disease.Immunity & ageing : I & A · 2022Review
- TNF-α Triggers RIP1/FADD/Caspase-8-Mediated Apoptosis of Astrocytes and RIP3/MLKL-Mediated Necroptosis of Neurons Induced by Angiostrongylus cantonensis Infection.Cellular and molecular neurobiology · 2022Article
- Regulated necrosis, a proinflammatory cell death, potentially counteracts pathogenic infections.Cell death & disease · 2022Review
- Identification of a pyroptosis related gene signature for predicting prognosis and estimating tumor immune microenvironment in bladder cancer.Translational cancer research · 2022Article
- Article
- Synaptic loss and progression in mice infected with Angiostrongylus cantonensis in the early stage.Journal of neuroinflammation · 2022Article
- Necroptosis in CNS diseases: Focus on astrocytes.Frontiers in aging neuroscience · 2022Review
- CXFrontiers in cellular and infection microbiology · 2021Article
- Chemoprevention of DMH-Induced Early Colon Carcinogenesis in Male BALB/c Mice by Administration ofMicroorganisms · 2020Article
- Angiostrongylus cantonensis causes cognitive impairments in heavily infected BALB/c and C57BL/6 mice.Parasites & vectors · 2020Article
- Mesenchymal stem cells combined with albendazole as a novel therapeutic approach for experimental neurotoxocariasis.Parasitology · 2020Article
- Angiostrongylus cantonensis Galectin-1 interacts with Annexin A2 to impair the viability of macrophages via activating JNK pathway.Parasites & vectors · 2020Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundAngiostrongylus cantonensis has been the only parasite among Angiostrongylidae to cause human central nervous system infection characterized by eosinophilic meningitis or meningoencephalitis. The mechanism of the extensive neurological impairments of hosts caused by A. cantonensis larvae remains unclear. The aim of the present study was to investigate apoptosis, necroptosis and autophagy in the brains of mice infected with A. cantonensis, which will be valuable for better understanding the pathogenesis of angiostrongyliasis cantonensis.
methodsFunctional and histological neurological impairments of brain tissues from mice infected with A. cantonensis were measured by the Morris water maze test and haematoxylin and eosin (H&E) staining, respectively. The transcriptional and translational levels of apoptosis-, necroptosis- and autophagy-related genes were quantified by quantitative real-time polymerase chain reaction (RT-PCR), and assessed by western blot and immunohistochemistry (IHC) analysis. Apoptotic and necroptotic cells and their distributions in infected brain tissues were analysed by flow cytometry and transmission electron microscopy (TEM).
resultsInflammatory response in the central nervous system deteriorated as A. cantonensis infection evolved, as characterized by abundant inflammatory cell infiltration underneath the meninges, which peaked at 21 days post-infection (dpi). The learning and memory capacities of the mice were significantly decreased at 14 dpi, indicating prominent impairment of their cognitive functions. Compared with those of the control group, the mRNA levels of caspase-3, -4, -6, and RIP3 and the protein levels of caspase-4, cleaved caspase-3, cleaved caspase-6, RIP3, and pRIP3 were obviously elevated. However, no changes in the mRNA or protein levels of FADD, Beclin-1 or LC3B were evident, indicating that apoptosis and necroptosis, but not autophagy, occurred in the brain tissues of mice infected with A. cantonensis. The quantitative RT-PCR, western blot, IHC, flow cytometry and TEM results further revealed the apoptotic and necroptotic microglia, astrocytes and neurons in the parenchymal and hippocampal regions of infected mice.
conclusionsTo our knowledge, we showed for the first time that A. cantonensis infection causes the apoptosis and necroptosis of microglia and astrocytes in the parenchymal and hippocampal regions of host brain tissues, further demonstrating the pathogenesis of A. cantonensis infection and providing potential therapeutic targets for the management of angiostrongyliasis.
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