Abstract
Some patients infected with the parasite Try-panosoma cruzi develop chronic Chagas' disease, while others remain asymptomatic for life. Although pathological mechanisms that govern disease progression remain unclear, the balance between degeneration and regeneration in the peripheral nervous system seems to contribute to the different clinical outcomes. This review focuses on certain new aspects of host-parasite interactions related to regeneration in the host nervous system induced by the trans-sialidase of T. cruzi, also known as a parasite-derived neurotrophic factor (PDNF). PDNF plays multiple roles in T. cruzi infection, ranging from immunosuppression to functional mimicry of mammalian neurotrophic factors and inhibition of apoptosis. PDNF affinity to neurotrophin Trk receptors provide sustained activation of cellular survival mechanisms resulting in neuroprotection and neuronal repair, resistance to cytotoxic insults and enhancement of neuritogenesis. Such unique PDNF-elicited regenerative responses likely prolong parasite persistence in infected tissues while reducing neuropathology in Chagas' disease.
Highlights
Despite recent progress in the control of Chagas’ disease, it is estimated that approximately 8 million people remain chronically infected with Trypanosoma cruzi, the etiological agent of the disease
Given that an additional 20% of the population is at risk of infection in endemic countries [57], Chagas’ disease (CD) remains a significant health problem in Latin America
The discovery of parasite-derived neurotrophic factor (PDNF) specific affinity to Trk receptors of mammalian neurotrophins pointed to a new direction in T. cruzi research, suggesting a possible mechanism for the parasite involvement in regeneration of mammalian nervous tissue
Summary
Despite recent progress in the control of Chagas’ disease, it is estimated that approximately 8 million people remain chronically infected with Trypanosoma cruzi, the etiological agent of the disease. Many of these infected individuals (30–40%) will develop life-threatening heart or gastrointestinal pathology. Survivors of the acute disease do not develop clinical symptoms for many years, and approximately 60–70% of them remain in the chronic indeterminate. Chuenkova and PereiraPerrin (asymptomatic) stage of the disease for life, while the other 30–40% will exhibit chronic symptomatic CD affecting peripheral nervous system (PNS) in the heart and digestive tract several years or even decades after the initial infection [6,66]. Analysis of T. cruzi interaction with CNS and PNS in the heart and gastrointestinal tract (GI) can provide some clues for the understanding of CD progression from benign to pathological form and ideas for possible therapeutic intervention
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