Apoptosis of mouse hippocampal cells induced by Taenia crassiceps metacestode factor

Abstract

Seizures, headache, depression and neurological deficits are the signs and symptoms most frequently reported in human neurocysticercosis. However, the cause of the associated learning and memory deficits is unknown. Here, we used Taenia crassiceps infection in mice as a model of human cysticercosis. The effects of T. crassiceps metacestode infection or T. crassiceps metacestode factor (MF) treatment on mouse hippocampal cells were studied; control mice were included. At 45 days after infection or treatment of the mice with MF, all mice were anaesthetized and perfused transcardially with saline followed by phosphate-buffered 10% formalin. Then the brains were carefully removed. Coronal sections stained using several techniques were analysed. Extensive and significant apoptosis was found in the experimental animals, mainly in the dentate gyrus, CA1, CA2, CA3 and neighbouring regions, in comparison with the apparently intact cells from control mice (P < 0.01). These results suggest that neurological deficits, especially the learning and memory deficits, may be generated by extensive apoptosis of hippocampal cells.

Experimental neurocysticercosis: absence of IL-4 induces lower encephalitis

“…All the control animals showed discrete levels of edema and hyperemia due to the mechanical trauma of the inoculation of sterile saline solution. These discrete alterations in the control group have also been observed in other experimental NCC studies 6,13,18,21 . In the infected animals, the majority of the cysticerci were located inside the lateral ventricles accompanied by a discrete-to-moderate intensity of inflammatory response.…”

“…This fact was previously reported in studies that showed that the mere presence of the parasite's antigens are responsible for the development of inflammatory alterations and ventriculomegaly, which may lead to cerebrospinal fluid obstruction 22,23 . Zepeda et al 21 showed that T. crassiceps antigens are able to induce inflammation in the brain tissue and apoptosis of hippocampal cells. Histological studies have shown that viable cysticerci, such as the ones in our study, have little or no surrounding inflammation in humans and pigs; while degenerating or dead cysticerci, which were not found in our study, had an inflammatory response in their surroundings 24 .…”

The Association Between Neurocysticercosis and Hippocampal Atrophy is Related to Age

“…24 In another murine model, intraperitoneal inoculation of Taenia crassiceps metacestode factor (a parasite akin to Taenia solium) in a mice model induces apoptosis of hippocampal cells due to complex inflammatory mechanisms. 25 The low prevalence of individuals with recurrent seizures in our series would favor the above-described seizure-independent inflammatory hypothesis, although we cannot rule out the presence of subclinical paroxysmal activity. Strengths of the present study include the unbiased selection of participants, the homogeneous characteristics of Atahualpa residents regarding race/ethnicity and living habits, the case-control design, and the high rates of interrater agreement for both CT and MRI readings.…”

Apoptosis and necroptosis of mouse hippocampal and parenchymal astrocytes, microglia and neurons caused by Angiostrongylus cantonensis infection

“…Disruption of the endothelium via apoptosis leads to the leakage of red blood cells, ring haemorrhage, and activated coagulation in adjacent nervous tissue in cerebral malaria [ 6 ]. In neurocysticercosis, neurological deficits, particularly learning and memory deficits, are generated by the extensive and significant apoptosis of hippocampal cells [ 7 ] and apoptosis of CD3+ T lymphocytes in the brains of hosts induced by T. solium cysticerci may be a mechanism by which the parasite downregulates its host’s cellular immune response during early cysticercosis [ 8 ]. The most common presentation of cerebral toxoplasmosis in HIV-infected patients is mass lesions consisting of well-defined areas of coagulative necroptosis with or without haemorrhage [ 9 ].…”