| Literature DB >> 16428768 |
Angela E Fritzinger1, Denise M Toney, Rebecca C MacLean, Francine Marciano-Cabral.
Abstract
Naegleria fowleri, the causative agent of primary amebic meningoencephalitis, is resistant to complement lysis. The presence of a complement regulatory protein on the surface of N. fowleri was investigated. Southern blot and Northern blot analyses demonstrated hybridization of a radiolabeled cDNA probe for CD59 to genomic DNA and RNA, respectively, from pathogenic N. fowleri. An 18-kDa immunoreactive protein was detected on the membrane of N. fowleri by Western immunoblot and immunofluorescence analyses with monoclonal antibodies for human CD59. Complement component C9 immunoprecipitated with the N. fowleri "CD59-like" protein from amebae incubated with normal human serum. In contrast, a gene or protein similar to CD59 was not detected in nonpathogenic, complement-sensitive N. gruberi amebae. Collectively, our studies suggest that a protein reactive with antibodies to human CD59 is present on the surface of N. fowleri amebae and may play a role in resistance to lysis by cytolytic proteins.Entities:
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Year: 2006 PMID: 16428768 PMCID: PMC1360335 DOI: 10.1128/IAI.74.2.1189-1195.2006
Source DB: PubMed Journal: Infect Immun ISSN: 0019-9567 Impact factor: 3.441