Suppression of humoral immunity and lymphocyte responsiveness during experimental trypanosoma cruzi infections

O'Daly, José A.; Simonis, Simonetta; Rolo, Nelva De; Caballero, Henry

doi:10.1590/s0036-46651984000200001

Cited by 14 publications

(3 citation statements)

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“…9, 20]. appearance of cytotoxic T ceils (CTL) in the spleen, lymph nodes and blood [17], impaired interleukin-2 (IL-2) production by splenocytes [6,7,27], and decreased lymphocyle proliferalive responses [4,6,1,10,19,21], paralleling a strongly reduced expression of IL-2 receptors [2], Moreover, recent studies on the phenotype of T cells in the spleen revealed an augumentation in the absolute numbers of CD4'CD8-and CD4 CD8* [18] as well as CD3'CD4 CD8- [16] Teells, thus showing an imbalance in the T-celi compartment, likely accompanied by polyclonal activation.…”

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confidence: 99%

Studies on the Thymus in Chagas' Disease II. Thymocyte Subset Fluctuations in Trypanosoma cruzi‐infected mice: Relationship to Stress

Moraes

Hontebeyrie-Joskowicz

Leboulenger³

et al. 1991

Scand J Immunol

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Changes in thymic T-cell subsets in mice acutely infected with Trypanosoma cruzi have been studied in both C3H/HeJ and C57BL/6 mice. The significant decrease in thymocyte number, observed in both mouse strains on day 14 post-infection correlated with a drastic decrease in CD4+CD8+ cell number, whereas the number of CD4-CD8-, CD4+CD8- and CD4-CD8+ cells remained essentially unchanged. The important increase in CD3hi cell frequency confirmed that resistant thymocytes during Chagas' disease development were mostly medullary thymocytes, whereas the thymic cortex was largely depleted, as previously observed on thymus sections. This involution of the thymus could have been due to the increase of circulating glucocorticoid levels observed after infection. However, similar cell modifications were found in infected adrenalectomized mice whose serum corticosterone levels were only slightly augmented. Thus, the thymic alterations appear not to be linked to stress responses, at least those dependent on high levels of circulating glucocorticoids.

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confidence: 99%

Studies on the Thymus in Chagas' Disease II. Thymocyte Subset Fluctuations in Trypanosoma cruzi‐infected mice: Relationship to Stress

Moraes

Hontebeyrie-Joskowicz

Leboulenger³

et al. 1991

Scand J Immunol

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“…Mice were randomly divided into two groups: Group A (Control) that were not inoculated with T. cruzi and Group B (infected mice) were infected intraperitoneally with 5x10 -2 blood-form trypomastigotes of the Y strain of T. cruzi ( O’Daly et al., 1984 ). The Y strain of T. cruzi was originally obtained from patients in Brazil and was kindly provided by Dr. Jose O’Daly, who has maintained the strain over the years through serial passages in homozygous C57B1/6 mice.…”

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confidence: 99%

The Role of the Na+/Ca2+ Exchanger in Aberrant Intracellular Ca2+ in Cardiomyocytes of Chagas-Infected Rodents

López

Linares

Adams

et al. 2022

Front. Cell. Infect. Microbiol.

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Chagas disease is produced by the parasite Trypanosoma cruzi (T. cruzi), which is the leading cause of death and morbidity in Latin America. We have shown that in patients with Chagas cardiomyopathy, there is a chronic elevation of diastolic Ca2+ concentration ([Ca2+]d), associated with deterioration to further address this issue, we explored the role Na+/Ca2+ exchanger (NCX). Experiments were carried out in noninfected C57BL/6 mice and infected with blood-derived trypomastigotes of the T. cruzi Y strain. Anesthetized mice were sacrificed and the cardiomyocytes were enzymatically dissociated. Diastolic [Ca2+] ([Ca2+]d) was measured using Ca2+ selective microelectrodes in cardiomyocytes from control mice (CONT) and cardiomyocytes from T. cruzi infected mice in the early acute phase (EAP) at 20 dpi, in the acute phase (AP) at 40 dpi, and in the chronic phase (CP) at 120 dpi. [Ca2+]d was 1.5-times higher in EAP, 2.6-times in AP, and 3.4-times in CP compared to CONT. Exploring the reverse mode activity of NCX, we replaced extracellular Na+ in equivalent amounts with N-methyl-D-glucamine. Reduction of [Na+]e to 65 mM caused an increase in [Ca2+]d of 1.7 times in cardiomyocytes from CONT mice, 2 times in EAP infected mice, 2.4 times in AP infected mice and 2.8 in CP infected mice. The Na+ free solution caused a further elevation of [Ca2+]d of 2.5 times in cardiomyocytes from CONT, 2.8 times in EAP infected mice, 3.1 times in AP infected mice, and 3.3 times in CP infected mice. Extracellular Ca2+ withdrawal reduced [Ca2+]d in both CONT and cardiomyocytes from Chagas-infected mice and prevented the increase in [Ca2+]d induced by Na+ depletion. Preincubation with 10µM KB-R7943 or in 1µM YM-244769 reduced [Ca2+]d in cardiomyocytes from infected mice, but not control mice. Furthermore, both NCX blockers prevented the increase in [Ca2+]d associated with exposure to a solution without Na+. These results suggest that Ca2+ entry through the reverse NCX mode plays a significant role in the observed [Ca2+]d dyshomeostasis in Chagas infected cardiomyocytes. Additionally, NCX inhibitors may be a viable therapeutic approach for treating patients with Chagas cardiomyopathy.

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“…The acute phase of infection with Trypanosoma cruzi is accompanied by immunosuppression, but its timing and the underlying mechanism are still a point of debate (Clinton et al 1975, Ramos et al 1978, Hayes & Kierszenbaum 1981, Harel-Bellan et al 1983, O'Daly et al 1984, Tarleton 1988a. The mechanisms implied in suppression are (1) a direct suppressive effect of the extracellular trypomastigote form on lymphocytes (Kierszenbaum & Sztein 1990); (2) the induction by trypomastigotes of suppressor cells, either lymphocytes (Ramos et al 1979, Tarleton 1988b or macrophages (Cunningham & Kuhn 1980a, Kierszenbaum 1982, Tarleton 1988b, Ritter & Kuhn 1990; (3) the production of other suppressive substances by splenocytes (Rottenberg et al 1989) or other cells (Cunningham & Kuhn 1980b, c).…”

Section: Introductionmentioning

confidence: 99%

Modulation of T‐cell responsiveness during Trypanosoma cruzi infection: analysis in different lymphoid compartments

Vandekerckhove

Darji²,

Rivera³

et al. 1994

Parasite Immunology

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Spleen and 1-ymph node cells of Trypanosoma cruziinfected mice were studied for mitogen-induced responsiveness in terms of proliferation and lymphokine production . Splenocyte ( S P ) as well as lymph node cell ( L N ) proliferation and IL-2 production were depressed during the acute phase of the infection. Proliferative capacity of L N cells recovered completely and that qf S P partially during the chronic phase. In contrast to these suppressive effects, the mitogen-induced IFN-gamma response was enhanced. In vitro co-incubation of normal S P or LN cells with trypomastigotes resulted in a reduced mitogen-induced cell proliferation and IL-2 secretion, similar to those seen with cells taken from infected mice. In contrast, trypomastigotes exerted a stimulatory activity on the rnitogen-induced IFN-gamma response of both S P and LN cells. Addition of lymph node cells from T. cruziinfected mice ( L N -I ) to lymph node cells of control mice ( L N-C) suppressed strongly the mitogen-induced responsiveness of such cocultures. A marginal level of suppression was recorded in cocultures of spleen cells from infectedmice (SP-I) and control spleen cells (SP-C). The potent suppressive cells within LN-Ipopulations were identified as macrophage-like and such cells were absent in SP-C and peritoneal exudate cells from T. cruzi infected animals.

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Suppression of humoral immunity and lymphocyte responsiveness during experimental trypanosoma cruzi infections

Cited by 14 publications

References 16 publications

Studies on the Thymus in Chagas' Disease II. Thymocyte Subset Fluctuations in Trypanosoma cruzi‐infected mice: Relationship to Stress

Studies on the Thymus in Chagas' Disease II. Thymocyte Subset Fluctuations in Trypanosoma cruzi‐infected mice: Relationship to Stress

The Role of the Na+/Ca2+ Exchanger in Aberrant Intracellular Ca2+ in Cardiomyocytes of Chagas-Infected Rodents

Modulation of T‐cell responsiveness during Trypanosoma cruzi infection: analysis in different lymphoid compartments

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