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Macrophageal/microglial cell activation and cerebral injury induced by excretory–secretory products secreted by Paragonimus westermani

 Jae-Chul Lee  ;  Geum-Sil Cho  ;  Jae Hyun Kwon  ;  Myeong Heon Shin  ;  Ji Hyae Lim  ;  Won-Ki Kim 
 NEUROSCIENCE RESEARCH, Vol.54(2) : 133-139, 2006 
Journal Title
Issue Date
Animals ; Brain Diseases/chemically induced* ; Brain Diseases/pathology ; Cell Death/drug effects ; Dose-Response Relationship, Drug ; Enzyme Inhibitors/pharmacology ; Fluoresceins ; Fluorescent Dyes ; Guanidines/pharmacology ; Helminth Proteins/chemistry ; Helminth Proteins/pharmacology* ; Immunohistochemistry ; Macrophage Activation/drug effects* ; Macrophages/drug effects* ; Male ; Microinjections ; Neuroglia/drug effects* ; Nitric Oxide Synthase Type II/antagonists & inhibitors ; Organic Chemicals ; Paragonimus/chemistry* ; RNA/biosynthesis ; RNA/genetics ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction
Excretory–secretory product (ESP) ; Microglia ; Monocyte ; Astrocyte ; iNOS
Cerebral paragonimiasis causes various neurological disorders including seizures, visual impairment and hemiplegia. The excretory–secretory product (ESP) released by Paragonimus westermani has a cysteine protease activity and plays important roles in its migration in the host tissue and modulation of host immune responses. To gain more insight into the pathogenesis of ESP in the brain, we investigated the inflammatory reaction and cerebral injury following microinjection of ESP into rat striatum. The size of injury was maximally observed 3 days after microinjection of ESP and then declined to control levels as astrocytes have repopulated the injury. ED1-positive monocytes and microglia were confluently found inside the injury. The mRNA expression of inducible nitric oxide synthase (iNOS) occurred as early as 9 h after ESP injection and then declined to control levels within 1 day. The iNOS inhibitor aminoguanidine largely decreased the expression of iNOS but did not reduce the size of lesion caused by ESP. Interestingly, however, heat inactivation of ESP caused a decrease of injury formation with no altered expression of iNOS. The data indicate that ESP produces brain tissue injury by recruiting activated monocytes/microglia via heat-labile protease activity.
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1. College of Medicine (의과대학) > Dept. of Environmental Medical Biology (환경의생물학교실) > 1. Journal Papers
Yonsei Authors
Shin, Myeong Heon(신명헌) ORCID logo https://orcid.org/0000-0001-8207-6110
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