Development of Brain Injury in Mice by Angiostrongylus cantonensis Infection Is Associated with the Induction of Transcription Factor NF-κB, Nuclear Protooncogenes, and Protein Tyrosine Phosphorylation

Lee, Hsiu Hsiung; Shiow, S.J.; Chung, Hung-Chi; Huang, Chih Yang; Lin, Chiann Ling; Hsu, Jeng Dong; Shyu, Ling Yuh; Wang, Chau Jong

doi:10.1006/expr.2000.4530

Cited by 13 publications

(8 citation statements)

References 29 publications

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“…Infection of mice with A. cantonensis causes brain injury and increased expression of NF-κB in the brains of ICR [16] and BALB/c strains of mice [17]. Exposure of human bone marrow endothelial cells to Trypanosoma brucei gambiense induced NF-κB translocation to the nucleus and CNS barrier dysfunction [18].…”

Section: Discussionmentioning

confidence: 99%

Matrix Metalloproteinase-9 Leads to Claudin-5 Degradation via the NF-κB Pathway in BALB/c Mice with Eosinophilic Meningoencephalitis Caused by Angiostrongylus cantonensis

Chiu

Lai

2013

PLoS ONE

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The epithelial barrier regulates the movement of ions, macromolecules, immune cells and pathogens. The objective of this study was to investigate the role of the matrix metalloproteinase (MMP)-9 in the degradation of tight junction protein during infection with rat nematode lungworm Angiostrongylus cantonensis. The results showed that phosphorylation of IκB and NF-κB was increased in mice with eosinophilic meningoencephalitis. Treatment with MG132 reduced the phosphorylation of NF-κB and the activity of MMP-9, indicating upregulation of MMP-9 through the NF-κB signaling pathway. Claudin-5 was reduced in the brain but elevated in the cerebrospinal fluid (CSF), implying that A. cantonensis infection caused tight junction breakdown and led to claudin-5 release into the CSF. Degradation of claudin-5 coincided with alteration of the blood-CSF barrier permeability and treatment with the MMP inhibitor GM6001 attenuated the degradation of claudin-5. These results suggested that degradation of claudin-5 was caused by MMP-9 in angiostrongyliasis meningoencephalitis. Claudin-5 could be used for the pathophysiologic evaluation of the blood-CSF barrier breakdown and tight junction disruption after infection with A. cantonensis.

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Section: Discussionmentioning

confidence: 99%

Matrix Metalloproteinase-9 Leads to Claudin-5 Degradation via the NF-κB Pathway in BALB/c Mice with Eosinophilic Meningoencephalitis Caused by Angiostrongylus cantonensis

Chiu

Lai

2013

PLoS ONE

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“…Inflammation involves the sequential activation of signaling pathways leading to the production of both pro- and anti-inflammatory mediators. NF-κB is inferred to have an important role in the induction of pro-inflammatory gene expression and angiostrongyliasis meningitis [6, 25]. Histone deacetylase sirtuin-1 is an important transcriptional regulatory protein attributed to the inhibition of NF-κB and reduces eosinophil infiltration in angiostrongyliasis meningoencephalitis [26].…”

Section: Discussionmentioning

confidence: 99%

Proteasome serves as pivotal regulator in Angiostrongylus cantonensis-induced eosinophilic meningoencephalitis

et al. 2019

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Proteasome primarily degrades the unneeded or damaged proteins by proteolysis. Disruption of the brain barrier and its resulting meningoencephalitis caused by Angiostrongylus cantonensis are important pathological events in non-permissive hosts. In this study, the results showed upregulated proteasome during A . cantonensis infection. Occludin degradation and matrix metalloproteinase-9 (MMP-9) activity were significantly increased in infected mice than in uninfected mice. Moreover, confocal immunoflourescence microscopy showed that occludin was co-localized with MMP-9. The infected-mice were treated with proteasomal activity inhibitor MG132 by 1.5 and 3.0 mg/kg/day, which resulted in significantly reduced protein levels of phosphorylated IκBα ( P <0.05) compared with the untreated control. The phosphorylated nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) showed similar result. In addition, MMP-9 activity and occludin degradation were reduced because of MG132 treatment. These results suggested that the proteasome in A . cantonensis infection degraded phosphorylated IκBα, modulated phosphorylated NF-κB, and then regulated the activation of MMP-9 and occludin degradation. Proteasome alterations were presented in eosinophilic meningitis of BALB/c mice and may contribute to the pathophysiology of eosinophilic meningitis by increasing occludin degradation. This molecule would serve as pivotal regulator in A . cantonensis -induced eosinophilic meningoencephalitis.

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“…Some mitogen-activated protein kinases and transcription factor are found to increase significantly in the CSF of mice infected with A. cantonensis. 32,33 Those mediators are significant in infection inflammation that may be related to oxidant stress. However, further study using ROS scavengers in mice after infection with A. cantonensis is required to clarify the role of those mediators.…”

Section: Discussionmentioning

confidence: 99%

Kinetic change of oxidative stress in cerebrospinal fluid of mice infected withAngiostrongylus cantonensis

Chung

Wang

Chen³

et al. 2010

Redox Report

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The cerebrospinal fluid (CSF) of C57BL/6 mice infected with Angiostrongylus cantonensis was examined for kinetic changes in oxidative stress parameters, including reactive oxygen species (ROS), superoxide dismutase (SOD), catalase, malondialdehyde (MDA), 8-isoprostane, and 8-hydroxy-2'-deoxyguanosine (8-OHdG). The ROS increased gradually in the early stage of infection. During days 12-30 post-infection, the infected mice revealed ROS levels significantly higher than that in uninfected controls (P < 0.001). The ROS levels peaked at day 24 and then returned to that observed in uninfected controls at day 45 post-infection. The kinetics of MDA, 8-isoprostane, and 8-OHdG concentration changes observed in the CSF of the infected mice corresponded with kinetic changes in ROS levels. Thus, the excess ROS caused lipid peroxidation and DNA damage to cells in the central nervous system (CNS) of mice infected with A. cantonensis despite the increased antioxidant SOD and catalase enzyme activities during post-infection days 12-30. The oxidative stress in the CNS of C57BL/6 mice was apparently increased by diseases associated with A. cantonensis infection.

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Development of Brain Injury in Mice by Angiostrongylus cantonensis Infection Is Associated with the Induction of Transcription Factor NF-κB, Nuclear Protooncogenes, and Protein Tyrosine Phosphorylation

Cited by 13 publications

References 29 publications

Matrix Metalloproteinase-9 Leads to Claudin-5 Degradation via the NF-κB Pathway in BALB/c Mice with Eosinophilic Meningoencephalitis Caused by Angiostrongylus cantonensis

Matrix Metalloproteinase-9 Leads to Claudin-5 Degradation via the NF-κB Pathway in BALB/c Mice with Eosinophilic Meningoencephalitis Caused by Angiostrongylus cantonensis

Proteasome serves as pivotal regulator in Angiostrongylus cantonensis-induced eosinophilic meningoencephalitis

Kinetic change of oxidative stress in cerebrospinal fluid of mice infected withAngiostrongylus cantonensis

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