Naegleria fowleri Lysate Induces Strong Cytopathic Effects and Pro-inflammatory Cytokine Release in Rat Microglial Cells.
10.3347/kjp.2011.49.3.285
- Author:
Yang Jin LEE
1
;
Chang Eun PARK
;
Jong Hyun KIM
;
Hae Jin SOHN
;
Jinyoung LEE
;
Suk Yul JUNG
;
Ho Joon SHIN
Author Information
1. Department of Microbiology, and Department of Molecular Science and Technology, Ajou University School of Medicine, Suwon 443-721, Korea. hjshin@ajou.ac.kr
- Publication Type:Brief Communication ; Research Support, Non-U.S. Gov't
- Keywords:
Naegleria fowleri;
microglial cell;
pro-inflammatory cytokine;
cytotoxicity
- MeSH:
Animals;
*Cell Death;
Chromium Radioisotopes/metabolism;
Cytokines/*secretion;
Humans;
Microglia/cytology/immunology/*physiology;
Microscopy;
Naegleria fowleri/*pathogenicity;
Rats;
Staining and Labeling
- From:The Korean Journal of Parasitology
2011;49(3):285-290
- CountryRepublic of Korea
- Language:English
-
Abstract:
Naegleria fowleri, a ubiquitous free-living ameba, causes fatal primary amebic meningoencephalitis in humans. N. fowleri trophozoites are known to induce cytopathic changes upon contact with microglial cells, including necrotic and apoptotic cell death and pro-inflammatory cytokine release. In this study, we treated rat microglial cells with amebic lysate to probe contact-independent mechanisms for cytotoxicity, determining through a combination of light microscopy and scanning and transmission electron microscopy whether N. fowleri lysate could effect on both necrosis and apoptosis on microglia in a time- as well as dose-dependent fashion. A 51Cr release assay demonstrated pronounced lysate induction of cytotoxicity (71.5%) toward microglial cells by 24 hr after its addition to cultures. In an assay of pro-inflammatory cytokine release, microglial cells treated with N. fowleri lysate produced TNF-alpha, IL-6, and IL-1beta, though generation of the former 2 cytokines was reduced with time, and that of the last increased throughout the experimental period. In summary, N. fowleri lysate exerted strong cytopathic effects on microglial cells, and elicited pro-inflammatory cytokine release as a primary immune response.
