Histological description of tomographic images of Taenia solium cysticerci in pig brains

Aluja, Aline S. de; González, Dante; Carbajal, Jesos Rodríguez; Flisser, Ana

doi:10.1016/0899-7071(89)90062-4

Cited by 27 publications

(9 citation statements)

References 3 publications

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“…Neurocysticercosis (NCC) is the most common helminth infection affecting the central nervous system (CNS) (de Aluja, González, Rodríguez Carbajal, & Flisser, ; Escobar, Aruffo, Cruz‐Sánchez, & Cervos‐Navarro, ). While pigs are the natural host of Taenia solium cysticerci, humans may be accidentally infected following ingestion of T. solium eggs, which subsequently develop into cysticerci (Escobar et al, ; Nash & Garcia, ).…”

Section: Introductionmentioning

confidence: 99%

Blood–brain barrier disruption and angiogenesis in a rat model for neurocysticercosis

Carmen-Orozco

Dávila-Villacorta

Cauna

et al. 2018

J of Neuroscience Research

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Neurocysticercosis (NCC) is a helminth infection affecting the central nervous system caused by the larval stage (cysticercus) of Taenia solium. Since vascular alteration and blood-brain barrier (BBB) disruption contribute to NCC pathology, it is postulated that angiogenesis could contribute to the pathology of this disease. This study used a rat model for NCC and evaluated the expression of two angiogenic factors called vascular endothelial growth factor (VEGF-A) and fibroblast growth factor (FGF2). Also, two markers for BBB disruption, the endothelial barrier antigen and immunoglobulin G, were evaluated using immunohistochemical and immunofluorescence techniques. Brain vasculature changes, BBB disruption, and overexpression of angiogenesis markers surrounding viable cysts were observed. Both VEGF-A and FGF2 were overexpressed in the tissue surrounding the cysticerci, and VEGF-A was overexpressed in astrocytes. Vessels showed decreased immunoreactivity to endothelial barrier antigen marker and an extensive staining for IgG was found in the tissues surrounding the cysts. Additionally, an endothelial cell tube formation assay using human umbilical vein endothelial cells showed that excretory and secretory antigens of T. solium cysticerci induce the formation of these tubes. This in vitro model supports the hypothesis that angiogenesis in NCC might be caused by the parasite itself, as opposed to the host inflammatory responses alone. In conclusion, brain vasculature changes, BBB disruption, and overexpression of angiogenesis markers surrounding viable cysts were observed. This study also demonstrates that cysticerci excretory-secretory processes alone can stimulate angiogenesis.

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Section: Introductionmentioning

confidence: 99%

Blood–brain barrier disruption and angiogenesis in a rat model for neurocysticercosis

Carmen-Orozco

Dávila-Villacorta

Cauna

et al. 2018

J of Neuroscience Research

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“…Extravasation of vascular fluids around cysts, often revealed by contrast enhancement and/or edema in radiological imaging (computed tomography [CT] or MRI), appears to be a crucial element of the pathology around degenerating cysts and a feature of post-treatment pericystic inflammation [ 10 , 15 ]. Using extravasation of intravenously delivered Evans blue (EB) as a marker for vascular leakage in and around cysts [ 16 ], we investigated the relationship between vascular permeability around cysts and the induction of inflammatory pathways following treatment with anthelmintic drugs.…”

Section: Introductionmentioning

confidence: 99%

Post-treatment Vascular Leakage and Inflammatory Responses around Brain Cysts in Porcine Neurocysticercosis

et al. 2015

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Cysticidal treatment of neurocysticercosis, an infection of humans and pig brains with Taenia solium, results in an early inflammatory response directed to cysts causing seizures and focal neurological manifestations. Treatment-induced pericystic inflammation and its association with blood brain barrier (BBB) dysfunction, as determined by Evans blue (EB) extravasation, was studied in infected untreated and anthelmintic-treated pigs. We compared the magnitude and extent of the pericystic inflammation, presence of EB-stained capsules, the level of damage to the parasite, expression of genes for proinflammatory and regulatory cytokines, chemokines, and tissue remodeling by quantitative PCR assays between treated and untreated infected pigs and between EB-stained (blue) and non stained (clear) cysts. Inflammatory scores were higher in pericystic tissues from EB-stained cysts compared to clear cysts from untreated pigs and also from anthelmintic-treated pigs 48 hr and 120 hr after treatment. The degree of inflammation correlated with the severity of cyst wall damage and both increased significantly at 120 hours. Expression levels of the proinflammatory genes for IL-6, IFN-γ, TNF-α were higher in EB-stained cysts compared to clear cysts and unaffected brain tissues, and were generally highest at 120 hr. Additionally, expression of some markers of immunoregulatory activity (IL-10, IL-2Rα) were decreased in EB-stained capsules. An increase in other markers for regulatory T cells (CTLA4, FoxP3) was found, as well as significant increases in expression of two metalloproteases, MMP1 and MMP2 at 48 hr and 120 hr post-treatment. We conclude that the increase in severity of the inflammation caused by treatment is accompanied by both a proinflammatory and a complex regulatory response, largely limited to pericystic tissues with compromised vascular integrity. Because treatment induced inflammation occurs in porcine NCC similar to that in human cases, this model can be used to investigate mechanisms involved in host damaging inflammatory responses and agents or modalities that may control damaging post treatment inflammation.

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“…To complete its life cycle, the metacestode form must survive for months in the tissues of the intermediate host. Viable cysticerci from pig muscles have minimal surrounding inflammation, but dying cysts are associated with a chronic granulomatous reaction (2,3). Similarly, pigs vaccinated with parasite antigens have intense granulomatous inflammation around dying cysts (29).…”

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confidence: 99%

Granuloma cytokines in murine cysticercosis

et al. 1997

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Taenia solium, is one of the most common causes of seizures worldwide. The symptoms result from granulomatous inflammation associated with dying cyst forms of the parasite. Although the invasive larvae can be killed by immune serum plus complement, immunity to the cyst stage depends on a cellular response. This dichotomous immune response is reminiscent of the extremes of the immune response associated with T helper 1 (Th1) and Th2 cytokine profiles. To characterize the cytokine response in cysticercosis, granulomas were removed from the peritoneal cavity of mice infected with Taenia crassiceps cysts and examined for cytokine message by in situ hybridization using 35 S-labeled RNA probes. The granulomas were staged based on histologic appearance of the degenerating parasite. Message for gamma interferon (IFN-␥) was identified by light microscopy in 11 of the 12 granulomas, and interleukin-2 (IL-2) message was identified in 9 of the 12. By laser scanning confocal microscopy, significantly increased IFN-␥ and IL-2 pixel intensity was identified in nearly all of the granulomas from early histologic stages. Message for IL-4 was seen in 6 of the 12 granulomas. Only granulomas with complete destruction of the parasite architecture displayed more than minimal amounts of IL-4 message by light microscopy, and only 2 of 12 granulomas had IL-4 pixel intensity significantly above background. Only minimal amounts of IL-10 message were detected in 4 of 11 granulomas. Thus, early granulomas in cysticercosis are predominantly associated with a Th1 response, whereas later granulomas, in which parasite destruction is complete, have a mixture of Th1 and IL-4. The Th1 response appears to play an important role both in the pathogenesis of disease as well as in the clearing of the parasites, with IL-4 involved in downregulation of the initial response.

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Histological description of tomographic images of Taenia solium cysticerci in pig brains

Cited by 27 publications

References 3 publications

Blood–brain barrier disruption and angiogenesis in a rat model for neurocysticercosis

Blood–brain barrier disruption and angiogenesis in a rat model for neurocysticercosis

Post-treatment Vascular Leakage and Inflammatory Responses around Brain Cysts in Porcine Neurocysticercosis

Granuloma cytokines in murine cysticercosis

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