[Apoptosis, a protective mechanism for pathogens and their hosts].
In this review we summarize the great amount of recent information on the apoptosis in aspects of the host-parasite interaction. Although apoptosis is a form of programmed cell death which plays a pivotal role in normal tissue development a plethora of pathogens including parasitic protista and helminths are able to modulate host apoptosis pathways to their own advantage. Here in we present and discuss new research data and results describing the phenomenon as a process have been controlled by gene expression, biochemical reactions and receptor-ligand interactions at the cell membrane surface. Section 1 describes apoptosis as ongoing process in normal tissue development. Section 2 analyzes the role of apoptosis in outcome of infection and pathogenesis of several disorders evoked by viruses and bacteria. The cellular mechanisms of cell death during infection with unicellular parasites such as Leishmania sp. and Plasmodium sp. are described in Section 3. In the next paragraph the potency of parasitic protista and helmiths for modulation host apoptosis pathways to their own advantage is discussed. The involvement of apoptosis in immunoregulation of the host immune function was proposed as a one of possible mechanism in creation of the host-parasite relationship. The molecular and cellular mechanisms of parasite-induced immune response via apoptosis pathways are discussed. We conclude that novel strategies for the management of the host-parasite relationships need to be explained into the mechanisms by which parasites induced apoptosis in contribution to the activity of immune system of the host.
Donskow-Schmelter
Katarzyna
K
Zakład Parazytologii, Instytut Zoologii, Wydział Biologii, Uniwersytet Warszawski, ul. Miecznikowa 1, 02-096 Warszawa. zuzia@biol.uw.edu.pl
Doligalska
Maria
M
D000222:Adaptation, Physiological / Q000276:immunology; D000818:Animals; D017209:Apoptosis / Q000276:immunology* / Q000502:physiology; D056890:Eukaryota / Q000472:pathogenicity* / Q000502:physiology; D006373:Helminthiasis / Q000276:immunology* / Q000469:parasitology* / Q000473:pathology; D006376:Helminths / Q000472:pathogenicity* / Q000502:physiology; D006790:Host-Parasite Interactions / Q000276:immunology; D006801:Humans; D011528:Protozoan Infections / Q000276:immunology* / Q000469:parasitology* / Q000473:pathology; D015398:Signal Transduction