Immune response in mice immunized with acidic antigenic fractions from Trypanosoma cruzi cytosol

Gea, Susana; Gruppi, Adriana; Cerbán, Fabio M.; Palencia, María cristina Pistoresi de; Vottero-Cima, E

doi:10.1590/s0036-46651992000500003

Cited by 12 publications

(4 citation statements)

References 15 publications

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“…To carry this out, SMC from non-infected mice (NI) or 16 dpi mice, treated or not with 3-HK, were cultured with or without an extract of T. cruzi (F105) [19]. After 72 h, culture supernatants were collected and analyzed for IFN-γ, TNF, IL-1β, IL-12, IL-6, IL-4, IL-5, TGF-β and IL-10.…”

Section: Resultsmentioning

confidence: 99%

“…The epimastigote homogenate was centrifuged at 105,000 X g as described previously [19], and the supernatant was used for ELISA and in vitro cultures. The synthetic peptide R13 (EEEDDDMGFGLFD) corresponding to the C-terminal domain of T. cruzi P1 and P2 ribosomal P proteins [65] and the synthetic peptide H13 (EESDDDMGFGLFD) corresponding to the C-terminal domain of mammalian P1 and P2 proteins [66], were synthesized and linked to BSA using glutaraldehyde by the Neosystem (Strasbourg, France).…”

Section: Methodsmentioning

confidence: 99%

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3-Hydroxy Kynurenine Treatment Controls T. cruzi Replication and the Inflammatory Pathology Preventing the Clinical Symptoms of Chronic Chagas Disease

et al. 2011

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Background3-Hydroxy Kynurenine (3-HK) administration during the acute phase of Trypanosoma. cruzi infection decreases the parasitemia of lethally infected mice and improves their survival. However, due to the fact that the treatment with 3-HK is unable to eradicate the parasite, together with the known proapoptotic and immunoregulatory properties of 3-HK and their downstream catabolites, it is possible that the 3-HK treatment is effective during the acute phase of the infection by controlling the parasite replication, but at the same time suppressed the protective T cell response before pathogen clearance worsening the chronic phase of the infection. Therefore, in the present study, we investigated the effect of 3-HK treatment on the development of chronic Chagas’ disease.Principal FindingsIn the present study, we treated mice infected with T. cruzi with 3-HK at day five post infection during 5 consecutive days and investigated the effect of this treatment on the development of chronic Chagas disease. Cardiac functional (electrocardiogram) and histopathological studies were done at 60 dpi. 3-HK treatment markedly reduced the incidence and the severity of the electrocardiogram alterations and the inflammatory infiltrates and fibrosis in heart and skeletal muscle. 3-HK treatment modulated the immune response at the acute phase of the infection impairing the Th1- and Th2-type specific response and inducing TGF-β-secreting cells promoting the emergence of regulatory T cells and long-term specific IFN-γ secreting cells. 3-HK in vitro induced regulatory phenotype in T cells from T. cruzi acutely infected mice.ConclusionsOur results show that the early 3-HK treatment was effective in reducing the cardiac lesions as well as altering the pattern of the immune response in experimental Chagas’ disease. Thus, we propose 3-HK as a novel therapeutic treatment able to control both the parasite replication and the inflammatory response.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

3-Hydroxy Kynurenine Treatment Controls T. cruzi Replication and the Inflammatory Pathology Preventing the Clinical Symptoms of Chronic Chagas Disease

et al. 2011

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“…Blood samples were collected 50, 90, and 135 days post-infection, representing the acute, intermediate, and chronic phases of the experimental infection, respectively. These samples were then assayed for antibodies to 'cruzipain' antigen (see below), by ELISA (Gea et al 1992).…”

Section: Serologymentioning

confidence: 99%

Chronic indeterminate phase of Chagas’ disease: mitochondrial involvement in infection with two strains

et al. 2012

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Chagasic cardiopathy has become one of the most frequent causes of heart failure and sudden death, as well as one of the most common causes of cardio-embolic stroke in Latin America. The myocyte response to oxidative stress involves the progression of cellular changes, primarily targeting the mitochondria and modifying therefore the energy supply. In this paper we analysed the effect of the infection of mice with 2 different strains of Trypanosoma cruzi (Tulahuen and SGO Z12) in the chronic indeterminate stage (75 days post-infection), upon the structure and function of cardiac mitochondria. The structural results showed that 83% of the mitochondria from the Tulahuen-infected mice presented an increase in their matrix and 91% of the mitochondria from the SGO Z12-infected group showed a reduction in their diameter (P < 0.05). When the Krebs cycle and mitochondrial respiratory chain functionality was analysed through the measurement of the citrate synthase and complexes I to IV activity, it showed that their activity was altered in all cases in a similar manner in both infected groups. In this paper we have demonstrated that the chronic indeterminate phase is not 'silent' and that cardiac mitochondria are clearly involved in the genesis and progression to the chronic chagasic cardiopathy when different factors alter the host-parasite equilibrium.

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“…1 Beta receptor affinity (Kd) of non-infected mice (n=20), infected with T. cruzi (n=20) and infected and treated (n=160). Bars with different letters differ significantly (p<0.05) 90 dpi, by enzyme-linked immunosorbent assay (Gea et al 1992). Survival was monitored every day.…”

Section: Methodsmentioning

confidence: 99%

Association of clomipramine and allopurinol for the treatment of the experimental infection with Trypanosoma cruzi

et al. 2010

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We have previously shown that clomipramine and allopurinol used separately are effective in preventing chronic chagasic cardiomyopathy. The aim of the present study was to evaluate the effect of the association of clomipramine (Clo--5 mg/kg/day/90 days) and allopurinol (Allo--5, 10, or 15 mg/kg/day/90 days) for the treatment of experimental Chagas disease in the acute stage. Treatment effectiveness was evaluated through parasitemia, survival, electrocardiography, serology, and cardiac histopathology. Groups treated showed no electrocardiographic abnormalities, in contrast to those untreated which presented 25% of mice with conduction alterations. The myocardium of treated mice (Clo, Allo10+Clo, and Allo15+Clo) presented no structural alterations. Cardiac b-receptor affinity was preserved in mice treated with Clo or Clo+Allo at the different doses; receptor density of the Clo and Allo15+Clo groups did not differ from the non-infected group. Anti-cruzipain antibody levels were similar in treated and untreated groups. Survival was significantly increased in the treated groups (p < 0.05), with Clo and all the Clo+Allo groups presenting the highest rates. These results show that the association of clomipramine + allopurinol is effective for Chagas disease treatment and has the same effect as clomipramine alone.

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Immune response in mice immunized with acidic antigenic fractions from Trypanosoma cruzi cytosol

Cited by 12 publications

References 15 publications

3-Hydroxy Kynurenine Treatment Controls T. cruzi Replication and the Inflammatory Pathology Preventing the Clinical Symptoms of Chronic Chagas Disease

3-Hydroxy Kynurenine Treatment Controls T. cruzi Replication and the Inflammatory Pathology Preventing the Clinical Symptoms of Chronic Chagas Disease

Chronic indeterminate phase of Chagas’ disease: mitochondrial involvement in infection with two strains

Association of clomipramine and allopurinol for the treatment of the experimental infection with Trypanosoma cruzi

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