Experimental encephalitis caused by Taenia crassiceps cysticerci in mice

Abstract

<jats:p>OBJECTIVES: To present the experimental model of neurocysticercosis (NCC) caused by Taenia crassiceps cysticerci, to describe the inflammatory process, susceptibility, or resistance of BALB/c and C57BL/6 mice to this infection, and to describe the host-parasite relationship. METHODS: The animals were intracranially inoculated with initial stage T. crassiceps cysticerci. They were euthanized at 7, 30, 60, and 90 days after the inoculation. Their encephala were removed for the histopathologic analysis, classification of the parasites, and inflammatory lesions. RESULTS: Experimental NCC was observed on both mice lineages. BALB/c mice presented inflammatory lesions with greater intensity, inducing necrosis on late stage parasites, and with an acute inflammation pattern, while C57BL/6 mice showed greater capability on provoking early necrosis in the cysticerci, which showed a chronic inflammation pattern. CONCLUSIONS: This experimental model induced NCC on mice with characteristic inflammation and lesions. C57BL/6 mice were able to induce precocious necrosis of the parasites presenting inflammatory lesions with lower intensity.</jats:p>

Experimental neurocysticercosis: absence of IL-4 induces lower encephalitis

“…The intracranial infection of the animals was performed as described by Matos-Silva et al 6 . Briefly, the animals were weighed and anesthetized with 0.01ml/g of ketamine 10% and xilazine 2% intraperitoneal injection.…”

“…The NCC symptoms are caused by the host inflammatory response, immune response modulation, location of the parasite, evolutionary stage of the parasite, parasitic burden, as well as the mass effect induced by its growth, which results in a wide clinical and laboratory polymorphism challenging the diagnosis of this disease 3,4 . Experimental models have been used as important tools in the study and comprehension of the host-parasite relationship in human cysticercosis in several locations including the neurological one 5,6,7 . The most-used parasite in the experimental models is Taenia crassiceps cysticercus due to its rapid development cycle and its antigenic similarity with T. solium 7,8 .…”

“…Soon afterwards there is a strong Th2 polarization due to the immunoregulatory capacity of the parasite increasing serum levels of IgG and IgE as well as IL-4, IL-13 and IL-5, which inhibits the initial Th1 response and favors the growth of parasitic burden 7,8,10,11 . The experimental models exploring the neurological location of cysticerci are described using Mesocestoides corti 5,12,13 and T. crassiceps 6 . The model carried out with M. corti was used to describe the role of defense cells and cytokines in the host-parasite relationship 13 , the expression of Toll-like receptors 5 , the migration of leucocytes to the central nervous system, the junction complex proteins and the immune system evasion strategies 14 .…”

“…It has also already been described that T. crassiceps cysticerci are able to induce NCC in immunocompromised 16 and immunocompetent individuals 17 . In this model, the infected animals presented with tissue alterations and lesions such as encephalitis, perivasculitis, ventriculomegaly, ependymitis, meningitis, microgliosis accompanied by the parasite's death, and extraparenchymal and parenchymal inflammatory infiltration 6,18 . Other experimental models have been proposed but instead of using T. crassiceps cysticerci they performed an intracranial inoculation of T. solium oncospheres in rats 19 and in swine 20 .…”

Cysticercosis and the immunossupression: what are the mechanisms involved?

“…Also in this Issue, Matos-Silva et al 26 , from Federal University of Goiás, report the development of an experimental model to NC studies involving two mice lineages by using T. crassiceps cysticerci. The authors observed in this original study that C57BL/6 mice showed greater capability on provoking early necrosis in the cysticerci with a chronic inflammation pattern, while BALB/c mice showed necrosis on late stage parasites with an acute inflammation pattern.…”