ИСТИНА

Intracellular parasites are known to develop mechanisms promoting or inhibiting cell death. Eukaryotic pathogens were studied less than prokaryotes in this respect, but parasitic protists of the genera Theileria, Toxoplasma, Leishmania, Haplosporidium, and Perkinsus all have been shown to inhibit apoptosis in the infected cells. Likely, this mechanism of intracellular survival is explored also by microsporidia (M). Indeed, widely distributed ability of M to induce cell hypertrophy and increase the lifespan of infected cells, suggest potential to hijack the host cell cycle control pathways. Inhibition of apoptosis was first presumed basing on in vitro studies of Anncaliia algerae (Scanlon et al., 1999). Later, it was straightforwardly demonstrated that Encephalitozoon spp. down regulated caspase-3 expression in Vero cells and inhibited p53 translocation to the nucleus (del Aguila et al., 2006). Nosema ceranae prevented ventricular epithelium cells from apoptosis, which was confirmed by TUNEL and IFA with caspase-3 antibodies (Higes et al., 2013). N. bombycis suppressed mitochondrial apoptotic pathway in the infected BmN cells (He at al., 2015). In our experiments E. cuniculi and Vittaforma corneae inhibited staurosporine-induced apoptosis in THP-1 cell line. Lower levels of TUNEL staining and caspase-3 activity in infected vs. non-uninfected macrophages corroborated with the data of microarray analysis: anti-apoptosis genes including BLC2 and TP53, were up-regulated in macrophages infected with M, while pro-apoptosis genes such as FADD, CASP3, CD40LG and others, were up-regulated in the macrophages incubated with dead, but not live, organisms. Molecular mechanisms that M use to regulate host apoptosis are yet to be identified.