Abstract
BackgroundToxocariasis is a worldwide zoonotic parasitic disease mainly caused by Toxocara canis. Humans can be infected by accidental ingestion of T. canis embryonated ovum-contaminated food, water, or encapsulated larvae in paratenic hosts’ viscera or meat. Since humans and mice are paratenic hosts of T. canis, the wandering larvae might cause mechanical tissue damage and excretory-secretory antigens may trigger inflammatory injuries to local organs. Long-term residence of T. canis larvae in a paratenic host’s brain may cause cerebral toxocariasis (CT) that contributes to cerebral damage, neuroinflammation and neuropsychiatric disorders in mice and clinical patients. Since the hippocampus has been long recognized as being responsible for learning and memory functions, parasitic invasion of this site may cause neuroinflammatory and neurodegenerative disorders. The present study intended to assess pathological changes, expressions of neurodegeneration-associated factors (NDAFs), including transforming growth factor (TGF)-β1, S100B, glial fibrillary acidic protein (GFAP), transglutaminase type 2 (TG2), claudin-5, substance P (SP) and interleukin (IL)-1β, and the ubiquitin-proteasome system (UPS) function in the hippocampus and associated cognitive behavior in ICR mice orally inoculated with a high, medium or low-dose of T. canis embryonated ova during a 20-week investigation.ResultsResults indicated although there were insignificant differences in learning and memory function between the experimental mice and uninfected control mice, possibly because the site where T. canis larvae invaded was the surrounding area but not the hippocampus per se. Nevertheless, enhanced expressions of NDAF, persistent UPS impairment and excess amyloid β (Aβ) accumulation concomitantly emerged in the experimental mice hippocampus at 8, 16 and 20 weeks post-infection.ConclusionsWe thus postulate that progressive CT may still progress to neurodegeneration due to enhanced NDAF expressions, persistent UPS impairment and excess Aβ accumulation in the hippocampus.
Highlights
Toxocariasis is a worldwide zoonotic parasitic disease mainly caused by Toxocara canis
Our results suggest that ubiquitin-proteasome system (UPS) impairment and insoluble amyloid β (Aβ) aggregations occurred in the hippocampus of mice with prolonged T. canis infection, irrespective of the infective inoculum level
The present study found that transforming growth factor (TGF)-β1, Transglutaminase type 2 (TG2), S100B and glial fibrillary acidic protein (GFAP) were significantly elevated during early infection at 8 wpi (Fig. 5), which was similar to results of our previous study [16]
Summary
Toxocariasis is a worldwide zoonotic parasitic disease mainly caused by Toxocara canis. Humans can be infected by accidental ingestion of foods, water, or soil contaminated by T. canis embryonated ova or larvae encapsulated in the viscera or muscles of paratenic hosts e.g. chickens or lambs [2]. When paratenic hosts, including mice and humans, accidentally ingest infective T. canis ova or tissue-encapsulated larvae, third-stage T. canis larvae emerge from the eggs and penetrate through the submucosa of the small intestine to further migrate to the liver via the portal circulation; they subsequently further invade various internal organs such as the liver or lungs, causing visceral larva migrans (VLM), the eyes, causing ocular larva migrans (OLM), or the central nervous system (CNS) leading to neurotoxocariasis (NT) [2, 7]. The number of CT cases described in the literature is still small, which might be explained by humans harboring few Toxocara larvae in their brains, and the effects of brain involvement are too cryptic to be explained or observed in human CT [14]
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