Difference in susceptibility to lysis between clones of the Y strain of Trypanosoma cruzi

Braga, Érika Martins; Galvão, Lúcia Maria da Cunha; Chiari, Égler; Martins, Marta

doi:10.1590/s0074-02761993000400005

Cited by 7 publications

(4 citation statements)

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“…It has been shown that the susceptibility of T. cruzi to lysis by complement varies according to the strain [32]; complement lysis assays showed that the Colombian T. cruzi strain is more susceptible to lysis than the Y T. cruzi strain at all serum concentrations [33]. Indeed, even within the same strain, variations in susceptibility have been observed among different clones [34]. There are no reports of T. cruzi lysis by complement with Ninoa strain; in our study the results showed a high percentage of lysis, similar to other Mexican Trypanosoma cruzi isolates reported by other authors [32].…”

Section: Discussionmentioning

confidence: 99%

Specific humoral and cellular immunity induced by Trypanosoma cruzi DNA immunization in a canine model

Arce-Fonseca

Ballinas-Verdugo

Zenteno

et al. 2013

Vet Res

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Chagas disease has a high incidence in Mexico and other Latin American countries. Because one of the most important known methods of prevention is vector control, which has been effective only in certain areas of South America, the development of a vaccine to protect people at risk has been proposed. In this study, we assessed the cellular and humoral immune response generated following immunization with pBCSP and pBCSSP4 plasmids containing the genes encoding a trans-sialidase protein (present in all three forms of T. cruzi) and an amastigote specific glycoprotein, respectively, in a canine model. Thirty-five beagle dogs were divided randomly into 5 groups (n = 7) and were immunized twice intramuscularly with 500 μg of pBCSSP4, pBCSP, pBk-CMV (empty plasmid) or saline solution. Fifteen days after the last immunization the 4 groups were infected intraperitoneally with 500 000 metacyclic trypomastigotes. The fifth group was unimmunized/infected. The parasitaemia in the immunized/infected dogs was for a shorter period (14 vs. 29 days) and the parasite load was lower. The concentration of IgG1 (0.612 ± 0.019 O.D.) and IgG2 (1.167 ± 0.097 O.D.) subclasses was measured (absorbance) 15 days after the last immunization with both recombinant plasmids, the majority of which were IgG2. The treatment of parasites using the serum from dogs immunized with pBCSP and pBCSSP4 plasmids produced 54% (± 11.8) and 68% (± 21.4) complement-mediated lysis, respectively. At 12 h post immunization, an increase in cytokines was not observed; however, vaccination with pBCSSP4 significantly increased the levels of IFN-γ and IL-10 at 9 months post-infection. The recombinant plasmid immunization stimulated the spleen cell proliferation showing a positive stimulatory index above 2.0. In conclusion, immunization using both genes effectively induces a humoral and cellular immune response.

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Section: Discussionmentioning

confidence: 99%

Specific humoral and cellular immunity induced by Trypanosoma cruzi DNA immunization in a canine model

Arce-Fonseca

Ballinas-Verdugo

Zenteno

et al. 2013

Vet Res

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“…The Y strain of T. cruzi was used for all experiments. Trypomastigote forms were cultured and purified from monkey kidney epithelial cell line VERO, as previously described (Braga et al, 1993). Parasites were harvested after 6 days in culture, centrifuged at 150×g for 10 min at room temperature, counted in a Neubauer chamber, centrifuged at 450×g for 10 min at 4°C, suspended in 10% FBS supplemented 199 medium and used for infection of cultures and co-cultures.…”

Section: Parasitesmentioning

confidence: 99%

Interferon-γ induced nitric oxide mediates in vitro neuronal damage by Trypanosoma cruzi-infected macrophages

Almeida‐Leite

Galvão

Afonso

et al. 2007

Neurobiology of Disease

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Neuronal lesions and peripheral denervation in Chagas' disease are related to local inflammation; however, the pathogenic mechanisms of neuronal lesions in the heart and megavisceras are still unclear. We investigated the involvement of nitric oxide (NO) on neuronal lesion in co-cultures of neurons and macrophages. Trypanosoma cruzi-infected and interferon-gamma (IFN-gamma)-activated co-cultures of neurons and wild-type (WT) macrophages showed significant reduction of both neuronal survival and neurite density. These findings correlated with the levels of NO and the expression of inducible nitric oxide synthase (iNOS). Accordingly, neuronal survival rate in the co-cultures was recovered to control levels by treatment of the cultures with the iNOS inhibitor, aminoguanidine. Moreover, neither neuronal survival nor the neurite density was affected in the co-cultures when the macrophages were harvested from iNOS-deficient mice. These results demonstrate that iNOS-derived NO is the major molecule involved in neuronal damage mechanism in our in vitro model of Chagas' disease neuropathology.

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“…The T. cruzi strains DM28c ( T. cruzi I type) and Y ( T. cruzi II type) were used in infection experiments (Zingales, 2018 ). Trypomastigote forms were cultured and purified using kidney epithelial lineage (VERO) cells, as described previously (Braga et al, 1993 ). After 6 days of culture, the parasites collected were centrifuged at 150 G for 10 min at room temperature and counted in a Neubauer chamber, centrifuged at 450 G for 10 min at 4°C and suspended 90% DMEM medium in 10% fetal calf serum (FCS) and added to cultures.…”

Section: Methodsmentioning

confidence: 99%

Neuronal Parasitism, Early Myenteric Neurons Depopulation and Continuous Axonal Networking Damage as Underlying Mechanisms of the Experimental Intestinal Chagas' Disease

Ricci

Béla

Moraes

et al. 2020

Front. Cell. Infect. Microbiol.

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There is a growing consensus that the balance between the persistence of infection and the host immune response is crucial for chronification of Chagas heart disease. Extrapolation for chagasic megacolon is hampered because research in humans and animal models that reproduce intestinal pathology is lacking. The parasite-host relationship and its consequence to the disease are not well-known. Our model describes the temporal changes in the mice intestine wall throughout the infection, parasitism, and the development of megacolon. It also presents the consequence of the infection of primary myenteric neurons in culture with Trypanosoma cruzi (T. cruzi). Oxidative neuronal damage, involving reactive nitrogen species induced by parasite infection and cytokine production, results in the denervation of the myenteric ganglia in the acute phase. The long-term inflammation induced by the parasite's DNA causes intramuscular axonal damage, smooth muscle hypertrophy, and inconsistent innervation, affecting contractility. Acute phase neuronal loss may be irreversible. However, the dynamics of the damages revealed herein indicate that neuroprotection interventions in acute and chronic phases may help to eradicate the parasite and control the inflammatory-induced increase of the intestinal wall thickness and axonal loss. Our model is a powerful approach to integrate the acute and chronic events triggered by T. cruzi, leading to megacolon.

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Difference in susceptibility to lysis between clones of the Y strain of Trypanosoma cruzi

Cited by 7 publications

References 0 publications

Specific humoral and cellular immunity induced by Trypanosoma cruzi DNA immunization in a canine model

Specific humoral and cellular immunity induced by Trypanosoma cruzi DNA immunization in a canine model

Interferon-γ induced nitric oxide mediates in vitro neuronal damage by Trypanosoma cruzi-infected macrophages

Neuronal Parasitism, Early Myenteric Neurons Depopulation and Continuous Axonal Networking Damage as Underlying Mechanisms of the Experimental Intestinal Chagas' Disease

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