.Naegleria fowleri, a free-living amoeba that is found in diverse environmental
habitats, can cause an acute fulminating hemorrhagic meningoencephalitis, called
primary amoebic meningoencephalitis (PAM) in experimental animals and in
humans. Pathogenicity of N. fowleri may be induced by contact-dependent and
contact-independent mechanisms, and both mechanisms lead to death of host cells.
Several proteins secreted from N. fowleri are likely to be associated with contactindependent
pathogenic mechanism of the amoeba. The excretory and secretory
proteins of N. fowleri (Nf-ESPs) include phospholipase, proteases, peroxiredoxins
and thrombin receptor. However, the precise mechanism induced by Nf-ESPs in
PAM is not fully understood yet. In this study, the cytopathic changes and
inflammatory responses induced by Nf-ESPs were analyzed in BV2 microglial
cells. Several cytokines, particularly IL-1α and TNF- α were highly up-regulated
by Nf-ESPs. Also, activation of P38 and JNK was observed in BV2 cells treated
with Nf-ESPs. The results collectively suggest that Nf-ESPs may play an
important role in N. fowleri mediated-PAM through induction of inflammatory
response in microglial cells and activation of MAPKs signal pathway.
