Free-living amebae belonging to the genus Acanthamoeba are the causative ag
ents of granulomatous amebic encephalitis, a chronic progressive disease of
the central nervous system, and of amebic keratitis, a chronic eye infecti
on. Granulomatous amebic encephalitis occurs more frequently in immunocompr
omised patients while keratitis occurs in healthy individuals. The recent i
ncreased incidence in Acanthamoeba infections is due in part to infection i
n patients with acquired immune deficiency syndrome, while that for keratit
is is due to the increased use of contact lenses. Understanding the mechani
sm of host resistance to Acanthamoeba is essential since the amebae are res
istant to many therapeutic agents. Studies in our laboratory as well as fro
m others have demonstrated also that microglial cells, resident macrophages
of the brain, elicit cytokines in response to A. castellanii. Neonatal rat
cortical microglia from Sprague-Dawley rats co-cultured with A. castellani
i produced mRNA for the inflammatory cytokines, interleukin 1 alpha, interl
eukin 1 beta, and tumor necrosis factor alpha. In addition, scanning and tr
ansmission electron microscopy revealed that microglia ingested and destroy
ed A. castellanii in vitro. These results implicate macrophages as playing
an effector role against Acanthamoeba and suggest immune modulation as a po
tential alternative therapeutic mode of treatment for these infections.