Programmed cell death in protozoa

Tijekom zadnjih 10-15 godina, znatan pomak je napravljen u razumijevanju kako pojedine programirane stanične smrti u parazitskim praživotinjama mogu utjecati na njihovu biologiju i njihove interakcije s domaćinima i vektorima. Pojava markera koji pokazuju apoptozu praživotinja ili autofagiju tijekom pojedinih procesa kao i funkcionalni dokazi su poduprli mišljenje da ove programirane stanične smrti igraju bitnu ulogu u načinu života parazitskih praživotinja. U suprotnosti, još nam je uvijek nepoznat učinak parazitske nekroze za parazitdomaćin interakcije i da li se on može pojaviti u reguliranom načinu kako je opisano kod višestaničnih organizama. Postoje dokazi da gustoća pojedinih parazita korelira s pojavom markera programirane stanične smrti. Mora se naglasiti, međutim, da definitivan dokaz koncepta regulacije gustoće parazita još uvijek nedostaje, posebno u uvjetima in vivo. Druga česta tema koja se pojavljuje iz navedenih primjera je da je autofagija uključena u diferencijaciju parazitskih praživotinja. Dodatno, autofagija i autofagijska stanična smrt su uobičajeni odgovori kada su paraziti izloženi okolišnom stresu. Autofagija u parazitskim praživotinjama, kao i u životinjama, primarno promiče opstanak, ali se može pretvoriti u programirani oblik smrti ako uvjeti okoliša premaše kapacitet stanice. Iako smo daleko od razumijevanja ovih procesa u potpunosti, apoptoza i autofagija su bitne kod parazitskih praživotinja i interakcija s njihovim domaćinima i vektorima. Detaljno znanje ovih mehanizama bi omogućilo efikasnu borbu protiv parazitskih praživotinja upotrebljavanjem njihovih vlastitih puteva smrti stanice.Over the past 10-15 years, considerable progress has been made in understanding how some of programmed cell death in parasitic protozoa may influence their biology and their interactions with hosts and vectors. The appereance of markers that show apoptosis or autophagy during certain processes and functional evidence support the view that this programmed cell death plays an important role in the lifestyle of parasitic protozoans. In contrast, the effect of parasitic necrosis of the parasite-host interactions and whether it can occur in a regulated manner as described in metazoa is still unknown. Now there is good evidence that the density of individual trypanosomatids and apicomplexan parasites correlates with the appearance of markers of programmed cell death. It should be noted, however, that definitive proof of the concept of regulation of parasite density by parasite apoptosis is still lacking, especially in vivo. Another common theme that appears from these examples is that autophagy is involved in differentiation of parasitic protozoans. In addition, autophagy and autophagic cell death are common responses when the parasites encounter environmental stress. It has become clear that autophagy in parasitic protozoa, as in metazoan, primarily promotes survival, but can be converted to a form of programmed cell death if environmental conditions exceed the capacity of cells. Although we are far from understanding these processes fully, apoptosis and autophagy are essential for the parasitic protozoa and interactions with their hosts and vectors. A detailed knowledge of the underlying molecular mechanism might open the possibility to combat protozoan parasites efficiently by promoting their own death pathways