Animal model of human disease with optic neuritis: neuropapillitis in a rat model infected with Angiostrongylus cantonensis

Feng, Ying; Zeng, Xiaofeng; Li, Weihua; Wang, Wencong; Ouyang, Liang; Sun, Xiao‐Feng; Lv, Ziquan; Wu, Zhongdao

doi:10.1007/s00436-014-4067-6

Cited by 5 publications

(5 citation statements)

References 23 publications

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“…The third-stage larvae of A.cantonensis were obtained from the infected Amazonian snail ( Ampullaria gigas ) by digestion of the snail tissue in artificial gastric juice (0.3 % pepsin, 0.7 % HCL and 10 ml/g tissue) at 37 °C for 2 h. The precipitates were then washed with distilled water, and the third-stage larvae were counted and collected by microscopy [ 22 ].…”

Section: Methodsmentioning

confidence: 99%

Preliminary expression profile of cytokines in brain tissue of BALB/c mice with Angiostrongylus cantonensis infection

Wei

et al. 2015

Parasites Vectors

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BackgroundAngiostrongylus cantonensis (A. cantonensis) infection can result in increased risk of eosinophilic meningitis. Accumulation of eosinophils and inflammation can result in the A. cantonensis infection playing an important role in brain tissue injury during this pathological process. However, underlying mechanisms regarding the transcriptomic responses during brain tissue injury caused by A. cantonensis infection are yet to be elucidated. This study is aimed at identifying some genomic and transcriptomic factors influencing the accumulation of eosinophils and inflammation in the mouse brain infected with A. cantonensis.MethodsAn infected mouse model was prepared based on our laboratory experimental process, and then the mouse brain RNA Libraries were constructed for deep Sequencing with Illumina Genome Analyzer. The raw data was processed with a bioinformatics’ pipeline including Refseq genes expression analysis using cufflinks, annotation and classification of RNAs, lncRNA prediction as well as analysis of co-expression network. The analysis of Refseq data provides the measure of the presence and prevalence of transcripts from known and previously unknown genes.ResultsThis study showed that Cys-Cys (CC) type chemokines such as CCL2, CCL8, CCL1, CCL24, CCL11, CCL7, CCL12 and CCL5 were elevated significantly at the late phase of infection. The up-regulation of CCL2 indicated that the worm of A. cantonensis had migrated into the mouse brain at an early infection phase. CCL2 could be induced in the brain injury during migration and CCL2 might play a major role in the neuropathic pain caused by A. cantonensis infection. The up-regulated expression of IL-4, IL-5, IL-10, and IL-13 showed Th2 cell predominance in immunopathological reactions at late infection phase in response to infection by A. cantonensis. These different cytokines can modulate and inhibit each other and function as a network with the specific potential to drive brain eosinophilic inflammation. The increase of ATF-3 expression at 21 dpi suggested the injury of neuronal cells at late phase of infection. 1217 new potential lncRNA were candidates of interest for further research.ConclusionsThese cytokine networks play an important role in the development of central nervous system inflammation caused by A. cantonensis infection.Electronic supplementary materialThe online version of this article (doi:10.1186/s13071-015-0939-6) contains supplementary material, which is available to authorized users.

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Section: Methodsmentioning

confidence: 99%

Preliminary expression profile of cytokines in brain tissue of BALB/c mice with Angiostrongylus cantonensis infection

Wei

et al. 2015

Parasites Vectors

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“…Some surveys showed that anti-inflammation or anti-helminthic treatment had no obvious effect on demyelination caused by A. cantonensis . We therefore investigated the impact of TSIIA combined with AB 2, 3 on demyelination caused by A. cantonensis . Previous studies showed that TSIIA can protect neurons from damage, including ganglion cells, dopaminergic neurons, hippocampal neurons, and cortical neurons 21-24.…”

Section: Discussionmentioning

confidence: 99%

“…We and others have previously shown that A. cantonensis infection leads to obvious demyelination of CNS in BALB/c mice 1, 2. Previous studies revealed that anti-helminthic treatment alone or in combination with corticosteroids had no obvious effect on demyelination caused by A. cantonensis 2, 3, suggesting that simple antiparasitic or/and suppression of inflammation is not sufficient . It is therefore necessary to identify more efficient treatment strategies to prevent demyelination associated with angiostrongyliasis.…”

Section: Introductionmentioning

confidence: 89%

Tanshinone IIA attenuates demyelination and promotes remyelination in A. cantonensis-infected BALB/c mice

Feng

Zheng

et al. 2019

Int. J. Biol. Sci.

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Background: Angiostrongylus cantonensis infection can cause demyelination in the central nervous system, and there is no effective treatment. Methods: We used dexamethasone, Tanshinone IIA (TSIIA) and Cryptotanshinone(Two traditional Chinese medicine monomers) in combination with albendazole (AB, a standard anti-helminthic compound) to observe their therapeutic effect on demyelination in A. cantonensis-infected mice. Luxol fast blue staining and electron microscope of myelin sheath, Oligodendrocyte (OL) number and myelin basic protein (MBP) expression in brain was detected in above groups. Results: TSIIA+AB facilitated OL proliferation and significantly increased both myelin sheath thickness and the population of small-diameter axons. In addition, TSIIA treatment inhibited the expression of inflammation-related factors (interleukin [IL]-6, IL-1β, tumor necrosis factor [TNF]-α, inducible nitric oxide synthase [iNOS]) rather than inhibiting eosinophil infiltration in brain. TSIIA also decreased microglial activation and shifted their phenotype from M1 to M2. Conclusions: Taken together, these results provide evidence that TSIIA combined with AB may be an effective treatment for demyelination caused by A. cantonensis infection and other demyelinating diseases.

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“…These findings underscore the need to identify more detailed pathogenesis. Infiltration of lymphocytes, macrophages, eosinophils and neutrophils is the dominant pathogenic manifestation of infected brain, not only that, demyelination is a typical injury which brings out limitation of nerve impulse conduction in which animal motor function is bound to be impacted [2,3,4].…”

Section: Introductionmentioning

confidence: 99%

Interleukin 17-producing γδ T cell induced demyelination of brain during Angiostrongylus cantonensis infection

Feng

Zhou

Zheng³

et al. 2020

Preprint

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Background: Angiostrongylus cantonensis infection is one typical reason of eosinophilic encephalitis (EM), which has been reported to induce serious damage in the central nervous system. Both parasite and host factors contribute to the onset of EM, but the related immune-inflammation pathogenesis remain poorly characterized.Methods: A. cantonensis infection model was generated through infecting mice by gavage. TEM and IF were used to assess the pathologic changes of brain. The mRNA expression of inflammatory factors was tested by qRT-PCR. Combining flow cytometry with western blotting to evaluate the alteration of inflammatory cells and related cytokines. Critical role of IL-17 was found, to evaluate the function of IL-17A, we injected IL-17A mAb to naive and A. cantonensis infected mice. Results: A. cantonensis larvae altered immune homeostasis in the brain, led to the destruction of myelin shealth and activation of microglia. IL-17A accumulation was observed, IL-17RA was expressed on oligodendrocyte and microglia during the infection. More important, γδ T cells are the source of IL-17A induced by parasite. After IL-17A neutralizing antibody was applied, alterations of microglia state and myelination were discorved, mice neurobehavioral test also improved.Conclusion: Our study reveals a previously unrecognized impact of the IL-17+ γδ T cells in parasitic encephalopathy and emphasizes that blocking IL17A signaling can attenuate microglia activation, thus reducing CNS demyelination and ameliorate behavioral deficit in A. cantonensis infected mice.

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Animal model of human disease with optic neuritis: neuropapillitis in a rat model infected with Angiostrongylus cantonensis

Cited by 5 publications

References 23 publications

Preliminary expression profile of cytokines in brain tissue of BALB/c mice with Angiostrongylus cantonensis infection

Preliminary expression profile of cytokines in brain tissue of BALB/c mice with Angiostrongylus cantonensis infection

Tanshinone IIA attenuates demyelination and promotes remyelination in A. cantonensis-infected BALB/c mice

Interleukin 17-producing γδ T cell induced demyelination of brain during Angiostrongylus cantonensis infection

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