Modulation of proteins in Naegleria fowleri amebae by bacteria

Naegleria fowleri are free‐living amebae found in soil and freshwater habitats that cause a fatal disease in humans called Primary Amoebic Meningoencephalitis. In the natural environment, amebae feed on bacteria. In the infected host, the amebae lyse and ingest nerve tissue. Proteins that lyse and degrade bacteria and mammalian cells have been described and are termed as naegleriapores or pore‐forming proteins (PFP). In order to prevent autolysis from PFPs, Naegleria may have developed mechanisms that enable the amebae to survive in the presence of cytolytic molecules. Recently, we have established that N. fowleri express a “CD59‐like” surface protein, but the function of this protein in amebae 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. Co‐culture of N. fowleri with log phase Escherichia coli or Pseudomonas aeruginosa resulted in differential expression of the “CD59‐like” protein. Treatment of the amebae with bacterial toxin also affected expression of the protein. Scanning and transmission electron microscopy demonstrated morphological changes in N. fowleri following co‐incubation with the bacteria. Under all conditions examined, the amebae remained intact and viable. The results of our study implicate a possible protective role of the “CD59‐like” protein in response to bacterial predators and bacterial toxins.