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Apoptosis induced by parasitic diseases

DOI: 10.1186/1756-3305-3-106

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Abstract:

Cell death by apoptotic-like mechanisms could be described as a ride to death with a return ticket, as initiation of the pathway may be reversed, with the potential that it could be manipulated for therapeutic purposes. The management of host-cell apoptosis could thus be an adjunctive factor for parasitic disease treatment. Evidence that the apoptotic process could be reversed by anti-apoptotic drugs has recently been obtained, leading to the possibility of host-cell rescue after injury. An important issue will be to predict the beneficial or deleterious effects of controlling human cell death by apoptotic-like mechanisms during parasitic diseases.Apoptosis is a form of programmed cell death involved in a wide range of adaptive processes, from embryogenesis to stress injury responses. The main benefits of apoptosis occur when an organism is uninfected. However, detrimental effects caused by apoptosis can be triggered by parasitic infection, depending upon the specific host-parasite situation. During their evolution, parasites have developed mechanisms to induce or avoid host cell apoptosis in order to be able to survive and complete their life cycle.Pathways involved in apoptosis are highly regulated, demonstrating that this mechanism is finely tuned according to the biological environment of the cell. Among the factors involved in that balance in infected organisms, the time of apoptosis (early or late occurrence), the cell type and the type of parasitism (intracellular or not) are the major modulators. For example, early apoptosis of host cells could contribute towards their fight against infection by intracellular parasites; equally, early apoptosis could favour the penetration of the parasite. Late apoptosis of cells of the defence system could be beneficial to the host, clearing excess cells and thereby avoiding the detrimental effects of excessive inflammatory response in the tissue that they would cause (e.g. the deleterious effect of reactive oxygen species

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