Is TNFα involved in early susceptibility of Trypanosoma cruzi-infected C3H/He mice?

Starobinas, Nancy; Russo, Marco; Minóprio, Paola; Hontebeyrie-Joskowicz, M.

doi:10.1016/0923-2494(91)90019-f

Cited by 46 publications

(34 citation statements)

References 13 publications

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“…TNF-α levels in serum and TNF-α mRNA in the heart tissue were increased during acute infection (28 dpi) and remained elevated throughout the chronic stage (120 dpi), as previously described (Starobinas et al 1991, dos Santos et al 2001). …”

Section: T Cruzi Infection Increases Expression Of Tnfr1mentioning

confidence: 59%

“…We observed an increase in TNFR1-bearing and TNF-α-expressing cells during infection of C57BL/6 mice with the low virulence Colombian strain of T. cruzi. TNF-α production was previously shown to be enhanced in T. cruzi-infected mice in association with susceptibility (Starobinas et al 1991), and in chronically infected patients in association with heart dysfunction (Ferreira et al 2003, Perez-Fuentes et al 2003. T. cruzi-derived molecules, including glycosylphosphaditidylinositolanchored mucins, have been shown to induce TNF-α production (Ropert et al 2002).…”

Section: Discussionmentioning

confidence: 99%

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TNF/TNFR1 signaling up-regulates CCR5 expression by CD8+ T lymphocytes and promotes heart tissue damage during Trypanosoma cruzi infection: beneficial effects of TNF-α blockade

Kroll-Palhares

Silvério

Silva

et al. 2008

Mem. Inst. Oswaldo Cruz

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Section: T Cruzi Infection Increases Expression Of Tnfr1mentioning

confidence: 59%

Section: Discussionmentioning

confidence: 99%

TNF/TNFR1 signaling up-regulates CCR5 expression by CD8+ T lymphocytes and promotes heart tissue damage during Trypanosoma cruzi infection: beneficial effects of TNF-α blockade

Kroll-Palhares

Silvério

Silva

et al. 2008

Mem. Inst. Oswaldo Cruz

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“…4,5 NO is synthesized in macrophages by inducible NO synthase (iNOS), which is induced by IFN-␥ acting synergistically with tumor necrosis factor (TNF)-␣. 6 Both of these cytokines are produced during the acute phase of T cruzi infection [7][8][9] concomitantly with an increase in the plasma concentration of nitrite, the end product of the activation of the L-arginine/NO pathway. 5 In addition to macrophages, many other cells are able to produce NO by use of the inducible or constitutive isoforms of the NO synthase (NOS) enzyme.…”

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confidence: 99%

Trypanosoma cruzi –Infected Cardiomyocytes Produce Chemokines and Cytokines That Trigger Potent Nitric Oxide–Dependent Trypanocidal Activity

Machado¹,

Martins²,

Aliberti³

et al. 2000

Circulation

225

216

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Background-The pathogenesis of myocarditis that occurs in Trypanosoma cruzi-infected mice is still poorly understood.Therefore, it is important to know the mediators that trigger leukocyte migration to the heart as well as the cellular source of these possible mediators. In this study, we investigated (1) NO synthase (NOS) induction, (2) NO synthesis, (3) trypanocidal activity, and (4) chemokine and cytokine mRNA expression by isolated cardiomyocytes infected with T cruzi. Methods and Results-Mouse cardiomyocytes were isolated, infected with T cruzi, and evaluated for induction of inducible NOS (iNOS), nitrite production, trypanocidal activity, and cytokine and chemokine mRNA expression. We found that T cruzi-infected murine embryonic cardiomyocytes produced nitrite and expressed mRNAs for the chemokines chemokine growth-related oncogene, monokine induced by interferon-␥, macrophage inflammatory protein-2, interferon-␥-inducible protein, RANTES, and monocyte chemotactic protein, for iNOS, and for the cytokines tumor necrosis factor (TNF)-␣ and interleukin (IL)-1␤. Separate addition of IL-1␤, interferon-␥, TNF-␣ or monocyte chemotactic protein, macrophage inflammatory protein-2, and interferon-␥-inducible protein, to cultured cardiomyocytes resulted in NO production but low trypanocidal activity. However, simultaneous addition of IL-1␤, interferon-␥, and TNF-␣ or the chemokines to cultures resulted in the induction of iNOS, high levels of nitrite, and a marked trypanocidal activity. The iNOS/L-arginine pathway mediated the latter activity, inasmuch as it was inhibited by treatment with N G -monomethyl-L-arginine. Conclusions-These results indicate that iNOS activation and the proinflammatory cytokines and chemokines produced by cardiomyocytes are likely to control parasite growth and cell influx, thus contributing to the pathogenesis of chagasic cardiomyopathy seen in T cruzi-infected mice. (Circulation. 2000;102:3003-3008.)

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“…The general pattern is that of a higher resistance of B6 as compared to C3H/HeJ mice, but there are always exceptions to this rule (Allen et al, 1977, Soeiro et al, 2000. Differences in cytokine response (Starobinas et al, 1991, Silva et al, 1991 and T helper 1/T helper 2 (Th1/Th2) balance (Hondowicz et al, 1997) were ascribed as the basis for such differences, but components of the innate immune response were not completely investigated. Other differences, which were not yet directly correlated to their resistance to inflammatory response, were also reported between B6 and C3H/HeJ mice, such as normal ECG pattern (Postan et al, 1987) or different susceptibility to cadmium-induced toxicity (Shimada et al, 1997).…”

mentioning

confidence: 99%

Differential Expression of mRNA Coding for the Alpha-2-macroglobulin Family and the LRP Receptor System in C57BL/6J and C3H/HeJ Male Mice.

Soeiro

Paiva

Waghabi

et al. 2001

Cell Struct. Funct.

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ABSTRACT. Expression of mouse A2M (MAM), murinoglobulin (MUG), the A2M receptor or LDL-Receptor related protein (A2MR/LRP) and the Receptor Associated Protein (RAP) were measured by northern blotting of mRNA isolated from liver, heart and peritoneal macrophages from C3H/HeJ and C57BL/6J (B6) mice. Marked differences between males of the two mouse strains were observed for MAM and MUG mRNA levels in liver, which were reflected in plasma levels of both proteinase inhibitors, as confirmed by immune-electrophoresis. C3H/HeJ mice had higher levels of the MAM and MUG mRNA and their corresponding plasma proteins than B6 mice. B6 mice expressed higher levels of LRP mRNA relative to C3H/HeJ mice but had lower levels of RAP mRNA. LRP receptor activity, assayed by fluoresceinated-A2M binding, was higher in B6 cells. The present data contribute to the knowledge of genetic background characteristics among male mouse of these two strains, which can take part in many biological events such as lipid metabolism, inflammation and immune response to different infectious agents.

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Is TNFα involved in early susceptibility of Trypanosoma cruzi-infected C3H/He mice?

Cited by 46 publications

References 13 publications

TNF/TNFR1 signaling up-regulates CCR5 expression by CD8+ T lymphocytes and promotes heart tissue damage during Trypanosoma cruzi infection: beneficial effects of TNF-α blockade

TNF/TNFR1 signaling up-regulates CCR5 expression by CD8+ T lymphocytes and promotes heart tissue damage during Trypanosoma cruzi infection: beneficial effects of TNF-α blockade

Trypanosoma cruzi –Infected Cardiomyocytes Produce Chemokines and Cytokines That Trigger Potent Nitric Oxide–Dependent Trypanocidal Activity

Differential Expression of mRNA Coding for the Alpha-2-macroglobulin Family and the LRP Receptor System in C57BL/6J and C3H/HeJ Male Mice.

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