Interplay of hypoxia and host cells in the translocation, invasion and dissemination of Taenia solium in neurocysticercosis

Abstract

Neurocysticercosis, caused by the invasion of the central nervous system (CNS) by Taenia solium larvae, poses a significant global health burden. Despite its prevalence and severe neurological consequences, understanding of the molecular and signalling pathways facilitating parasite dissemination and CNS invasion is limited. The lack of comprehensive knowledge of host-parasite interactions and associated proteins involved in T. solium infection hinders the development of targeted interventions to mitigate its ability to cross the epithelia barrier. This is complicated by reduced oxygen availability in the intestine, a phenomenon called hypoxia. Hypoxia can result in epithelial barrier disruption and cell damage, thereby promoting the translocation and dissemination of T. solium. This study aims to establish the role of hypoxia in T. solium invasion and disseminated infections. The effect of hypoxia on the migration, viability and morphological characteristics of T. solium would be determined using transwell invasion assays, flow cytometry and microscopy. T. solium oncosphere development and dissemination under hypoxic and normoxic conditions will be monitored using animal models. Also, host-parasite transcriptome and proteome profiling will be performed to determine pathways triggered under hypoxic conditions. It is expected that hypoxia would promote the invasion and dissemination of T. solium by enhancing epithelial and endothelial cell permeability. , hypoxia will induce the expression of binding and adhesion proteins and other virulence markers such as enolase, serpin, and glutathione transferases that are involved in host invasion. Understanding the role of hypoxia in the translocation mechanism of T. solium can be leveraged to provide insights into host tissues dissemination and the development of appropriate interventions.