In:
The Journal of Immunology, The American Association of Immunologists, Vol. 178, No. 1_Supplement ( 2007-04-01), p. S99-S99
Abstract:
Naegleria fowleri, a free-living amoeba of soil, ponds, andfresh water, causes primary amoebic meningoencephalitis in humansand other mammals. Upon invasion in vivo, N. fowleri is capable of destructing or killing host cells by cytolysis. However, it is unknown on the mechanism by which N. fowleri induces host cell death. In this study, we investigated the mechanism of host cell death induced by N. fowleri. Incubation of Jurkat T cells with live trophozoites of N. fowleri resulted in cell death, as measured by LDH release assay or propidium iodide staining. In addition, N. fowleri induced DNA fragmentation in Jurkat cells in a time and dose-dependent manner. N. fowleri caused cleavage of calpain, caspase-3, and cytoskeletal proteins such as vinculin and paxillin. Pretreatment of cells with NADPH oxidase inhibitor DPI inhibited N. foweleri-induced apoptosis, whereas calpain inhibitor calpeptin or pan-caspase inhibitor z-VAD-fmk did not. When we incubated Jurkat cells with N. fowleri in a Transwell chamber (pore size 0.4 μm), comparable level of cell death rate was found compared to control without chamber, suggesting an important role of secretory factors in N. foweleri-induced cell death. Moreover, secretroy components released by N. fowleri induced host cell death, and heat treatment abolished host cell death by secretory components. These results suggest that heat labile proteins secreted by N. fowleri induce apoptotic cell death in Jurkat T cells.
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.178.Supp.51.13
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2007
detail.hit.zdb_id:
1475085-5
