Modulation of a "CD59-like" Protein in Naegleria fowleri Amebae by Bacteria

Found in soil and freshwater habitats, Naegleria fowleri are free-living amebae that cause a fatal disease in humans called Primary Amebic Meningoencephalitis. In the natural environment, amebae feed on bacteria. In the infected host, the amebae lyse and ingest nerve tissue. Recently, we have establ...

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Bibliographic Details
Published in:The Journal of eukaryotic microbiology 2004-09, Vol.51 (5), p.522-528
Main Authors: FRITZINGER, ANGELA E., MARCIANO-CABRAL, FRANCINE
Format: Article
Language:English
Subjects:
Acanthamoeba
Animals
bacterial toxin
CD59 Antigens - metabolism
Escherichia coli
Escherichia coli - metabolism
Humans
Mice
Naegleria fowleri - immunology
Naegleria fowleri - metabolism
Naegleria fowleri - ultrastructure
pore-forming protein
Pseudomonas aeruginosa
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Summary:Found in soil and freshwater habitats, Naegleria fowleri are free-living amebae that cause a fatal disease in humans called Primary Amebic Meningoencephalitis. In the natural environment, amebae feed on bacteria. In the infected host, the amebae lyse and ingest nerve tissue. Recently, we have established that N. fowleri expresses a "CD59-like" surface protein, but the function of this protein in the ameba has not been elucidated. In mammalian cells, CD59 is a complement-regulatory protein that inhibits complement-mediated lysis of cells expressing this protein. In the present study, expression of the "CD59-like" protein in response to bacteria and bacterial toxins was investigated by Western immunoblot analysis. Co-culture of N. fowleri with log phase Escherichia coli or Pseudomonas aeruginosa resulted in differential expression of the "CD59-like" protein. Co-cultures of amebae and bacteria were examined by electron microscopy. The results of our study implicate a possible protective role of the "CD59-like" protein in response to bacterial predators and bacterial toxins, because amebae remained intact after co-culture with bacteria.
ISSN:1066-5234
1550-7408
DOI:10.1111/j.1550-7408.2004.tb00287.x