Open Access
Review Article

Table 1

Cell death and host defense in hydatid cysts.

Cell death type Effects on host-pathogen interaction Consequences for host defense References
Apoptosis X-rays, carbon-ion, gamma irradiation, enhance of hydrogen peroxide and dexamethasone induces extensive DNA damage and apoptosis. Less immune pathology [24, 28, 30, 33, 53]
E. multilocularis live worm: Up-regulation of genes that support hepatocyte apoptosis such as Gadd45c, p21, p53, and cleaved-caspase3. Increase of immunodeficiency factors
Necrosis Releases of hydatic cyst fluid to extracyst space induce tissue necrosis. Unknown [26, 34, 58]
Some toxic substances have scolecidal effects.
Inflammation IgG and IgM increase inflammation in the germinal layer and laminated layer. Dextran sulfated sodium significantly reduces the levels of NO, IFN-γ, TNF-α and increases the production of IL-10 [13, 32, 41]
Dextran sulfated sodium can induce acute colitis.
Autophagy Albendazole and Metformin can increase metacestode tissue disruption with autophagosomes. Penetration on the laminated layer. Metacestodes from mice treated with Albendazole and Metformin showed complete tissue disruption with autophagosomes. [22, 23, 29]
TOR is an effective in vitro anti-echinococcosis agent that induces autophagy.
Bortezomib in the hydatid cyst can cause ER stress and provoke autophagy in protoscoleces.