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Vol. 11, Issue 4, 1487-1498, April 2000
Parasitology Research Center, Department of Pathology, Tufts
University School of Medicine, Boston, Massachusetts 02111
Despite the neuronal degeneration in the chronic stage of Chagas'
disease, neuron counts actually increase in the preceding, asymptomatic
stage, in contrast to the age-related decrease in neuron counts in
age-matched normal individuals. Relevant to this observation, we found
that the trans-sialidase (TS) of Trypanosoma cruzi, the etiologic agent of Chagas' disease, induces neurite outgrowth and rescues PC12 cells from apoptotic death caused by growth
factor deprivation. These properties, novel for a parasite protein,
were independent of catalytic activity and were mapped to the C
terminus of the catalytic domain of TS. TS activated protein
kinase Akt in a phosphoinositide-3 kinase-inhibitable manner,
suggesting a molecular mechanism for the TS-induced neuroprotection. TS
also triggered bcl-2 gene expression in growth factor-deprived cells,
an effect consistent with TS protecting against apoptosis. Ciliary
neurotrophic factor and leukemia inhibitory factor, two cytokines
critical to the repair of injured motor neurons, specifically potentiated the TS action. The results suggest that TS acts in synergy
with host ciliary neurotrophic factor or leukemia inhibitory factor to promote neuronal survival in T. cruzi-infected individuals.
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