Open Access
Review
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. |
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