Alterations of myelin proteins in inflammatory demyelination of BALB/c mice caused by Angiostrongylus cantonensis

Lin, Keh‐Liang; Chen, K.M.; Lan, Kuang-Ping; Lee, H.H.; Lai, Shih‐Chan

doi:10.1016/j.vetpar.2010.03.019

Cited by 16 publications

(18 citation statements)

References 31 publications

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“…Further studies are also required to resolve whether MBP production in oligodendroglial cells infected in A. cantonensisconditioned medium is also produced through the Erk1/2-NF-κB pathways. Based on our results presented here and in the previous study of Lin et al (17), we postulate that through blocked Erk1/2-NF-κB activity can improve MBP over-production and RSC96 Schwann cells damage.…”

Section: Discussionsupporting

confidence: 80%

“…In contrast, demyelination impairs nerve conduction, induces inflammatory cascade and causes axonal loss (5,21). Moreover, demyelination is often accompanied by MBP production: BALB/c mice infected with A. cantonensis elicit demyelination, which implicates alterations of myelin proteins, including MBP (17). Interestingly, we likewise found MBP production in RSC96 Schwann cells in response to treatment in A. cantonensis-conditioned culture medium in a timedependent manner.…”

Section: Discussionsupporting

confidence: 56%

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Angiostrongylus Cantonensis-Conditioned Culture Medium Induces Myelin Basic Protein Alterations via Erk1/2 and NF-κB Activation in Rat RSC96 Schwann Cells

et al. 2018

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Eating of excessive raw or undercooked environmental snails produces angiostrongyliasis demyelination caused by Angiostrongylus cantonensis (A. cantonensis). The aim of this study was to investigate the association between extracellular signal-regulated kinase (Erk)1/2-nuclear factor (NF)-κB pathway and myelin basic protein (MBP) expression in RSC96 Schwann cells treated with A. cantonensis-conditioned culture medium, which was prepared by culturing the third-stage (L3) nematode larvae in DMEM for 72 h. The supernatants were collected and filtered before use. Our results showed that MBP was produced in the RSC96 cells at 16 h to 48 h post-stimulation (PS). Phosphorylated (p)-NF-κB levels were significantly increased from 8 h to 48 h PS, as were the p-Erk1/2 levels at the same time points. Additionally, expression of p-NF-κB and MBP was significantly decreased by treatment with QNZ, an NF-κB inhibitor. Treatment with PD98059, an Erk kinase inhibitor, efficiently reduced p-Erk1/2, p-NF-κB and MBP expression in the Schwann cells. These results suggest that A. cantonensis-conditioned culture medium induced suppression of the Erk1/2-NF-κB signaling pathway leading to reduced MBP production in RSC96 Schwann cells. Thus, inhibiting this signaling intermediate involved in MBP expression may be a potential method for controlling inflammatory development of A. cantonensis-induced MBP changes in preceded demyelination.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionsupporting

confidence: 56%

Angiostrongylus Cantonensis-Conditioned Culture Medium Induces Myelin Basic Protein Alterations via Erk1/2 and NF-κB Activation in Rat RSC96 Schwann Cells

et al. 2018

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“…This is the first description of this process in experimental NCC. Lin et al 39 confirmed the destruction of the myelin sheath induced by a local inflammatory process related to the presence of a parasite, Angiostrongylus cantonensis. Also, the maintenance of the NCC inflammatory process has direct relation to the increase in the expression of VEGF (vascular endothelial growth factor), which facilitates the influx of immune cells 9,10 .…”

Section: Discussionmentioning

confidence: 96%

“…An experimental study described the infection of mice with Trichobilharzia regent (Schistosomatidae) and the histologic and immunohistochemical consequences of this infection. The authors described the axon injuries and demyelination to mechanical injury caused by the parasite's migration through the nervous tissue and not to the host's immune response 40 , while the experimental neurological infection with Angiostrongylus cantonensis (Strongylida) induces the release of inflammatory mediators, leading to intracerebral myelin breakdown, and increase in myelin proteins in the cerebrospinal fluid 39 .…”

Section: Discussionmentioning

confidence: 99%

Demyelination in experimental intraventricular neurocysticercosis

Moura

Milhomem

Lima

et al. 2020

Arq. Neuro-Psiquiatr.

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Neurocysticercosis (NCC) is classified as a neglected tropical disease, which affects mainly Latin America and Africa in spite of some reports in North America and Europe. NCC represents the cause of up to 30% of the reported cases of epilepsy in endemic countries. The NCC injuries present direct relation to the development stage, location, and number of parasites as well as to the host immune response. This study aimed the characterization of the inflammatory response and tissue injuries by means of the analyses of the periventricular and parenchymatous demyelination through the experimental intraventricular NCC infection. Therefore, BALB/c mice were submitted to experimental NCC inoculation with Taenia crassiceps cysticerci. Their brains were removed at 7, 30, 60, and 90 days after the inoculation (DAI), and analyzed after staining with hematoxylin and eosin (HE), Luxol Fast Blue, and Nissl. It was possible to observe ventriculomegaly, inflammatory infiltration composed by polymorphonuclear and mononuclear cells, and foamy macrophages. The presence of inflammatory cells was associated with neurodegeneration detected by the areas with demyelination observed initially in the periventricular area and lately in the parenchyma. In conclusion, the presence of cysticerci and the consequent inflammation were able to promote initial periventricular demyelination followed by parenchymatous demyelination as the infection progressed.

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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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Alterations of myelin proteins in inflammatory demyelination of BALB/c mice caused by Angiostrongylus cantonensis

Cited by 16 publications

References 31 publications

Angiostrongylus Cantonensis-Conditioned Culture Medium Induces Myelin Basic Protein Alterations via Erk1/2 and NF-κB Activation in Rat RSC96 Schwann Cells

Angiostrongylus Cantonensis-Conditioned Culture Medium Induces Myelin Basic Protein Alterations via Erk1/2 and NF-κB Activation in Rat RSC96 Schwann Cells

Demyelination in experimental intraventricular neurocysticercosis

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

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