Project description:The cestode Taenia solium develops as a tapeworm in the human intestine, starting from a larva (cyst). Upon maturing, it produces hundreds of thousands of infectious eggs. When ingested by pigs and humans, the eggs develop as cysts that lodge in various tissues, including the brain, leading to neurocysticercosis. Despite advances in understanding cestode biology through genomic and transcriptomic studies, particularly in model organisms, much remains unknown about the activation of T. solium cysts in the human digestive tract and the events that drive the development into adult worms—the stage responsible for dispersing the parasite. We present a transcriptome generated by Next Generation Sequencing from T. solium cysts activated in culture and collected at three different in vitro growth stages, as defined by their morphology. We identified differentially expressed genes and biological processes relevant to growth phases that can be further explored with the dataset. The information is valuable for identifying genes that regulate the molecular, metabolic, and cellular events leading to parasite maturation or elements driving its transmission.
Project description:Subarachnoid neurocysticercosis (SANCC) is caused by an abnormally transformed form of the metacestode or larval form of the tapewormTaenia solium. In contrast to vesicular parenchymal and ventricular located cysts that contain a viable scolex and are anlage of the adult tapeworm, the subarachnoid cyst proliferates to form aberrant membranous cystic masses within the subarachnoid spaces that cause mass effects and acute and chronic arachnoiditis. How subarachnoid cyst proliferates and interacts with the human host is poorly understood, but parasite stem cells (germinative cells) likely participate. RNA-seq analysis of the subarachnoid cyst bladder wall compared to the bladder wall and scolex of the vesicular cyst revealed that the subarachnoid form exhibits activation of signaling pathways that promote proliferation and increased lipid metabolism. These adaptions allow growth in a nutrient-limited cerebral spinal fluid. In addition, we identified therapeutic drug targets that would inhibit growth of the parasite, potentially increase effectiveness of treatment, and shorten its duration.
Project description:This study aims to investigate the immunemodulatory effects of excretory-secretory products (ESPs) from the parasite Taenia solium on human macrophages to understand immunopathogenesis of neurocysticercosis (NCC). NCC is an infection of the central nervous system caused by the larvae of T. solium and is a major contributor to acquired epilepsy. Although ESPs from parasites are known to possess immune-modulating properties, the specific mechanisms of their action in NCC remains unclear. Therefore, this expression study seeks to shed light on the exact mechanism by which T. solium ESPs exert their immune-suppressive effects on human macrophages. Understanding this mechanism can provide valuable insights into the pathogenesis of NCC and potentially contribute to the development of novel therapeutic strategies for managing the disease. The study employed miRNA microarray technology to investigate the post-translational effects of excretory-secretory products (ESPs) from Taenia solium on human macrophage function. microRNAs, are small non-coding RNA molecules that play a crucial role in post-transcriptional gene regulation. The aim of study is to identify specific miRNAs that might be responsible for modulating macrophage function. Altered expression of miRNAs can influence the translation and stability of target mRNA molecules, subsequently affecting the production of proteins and the overall function of macrophages, thus affecting immune homeostasis in infection. Understanding the miRNA-mediated regulatory mechanisms involved in the immune response to T. solium infection can contribute to a better understanding of the pathogenesis of neurocysticercosis and potentially uncover novel therapeutic targets for managing the disease.