Trypanosoma cruzi:IL-10, TNF, IFN-γ, and IL-12 Regulate Innate and Acquired Immunity to Infection

Abrahamsohn, Ises de Almeida; Coffman, Robert L.

doi:10.1006/expr.1996.0109

Cited by 174 publications

(162 citation statements)

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“…Although it has been shown that IFN-␥ and/or TNF-␣ stimulate NO production by T. cruzi-infected macrophages (5,8,36), the possible stimulatory activity of IFN-I in this process had not hitherto been investigated. We show in the present study that, in addition to TNF-␣, IFN-I were produced by peritoneal cavity cells and by SC obtained from mice infected with T. cruzi (8 days of infection).…”

Section: Discussionmentioning

confidence: 99%

“…It was shown by Trischmann (29) that control of T. cruzi proliferation already occurs in the first cycles of intracellular replication, indicating the importance of innate immunity in parasitism control. Even mice completely devoid of functional T or B cells (RAG Ϫ/Ϫ ) can exert some control of parasitism by mechanisms that include NO production and depend on activation by IL-12, IFN-␥, and TNF-␣ (36). Both the control of parasitism and host survival are critically dependent on these cytokines because they are active as mediators of the innate, as well as of the acquired immunity, and because IL-12 and IFN-␥ are essential for mounting a protective Th1 response.…”

Section: Discussionmentioning

confidence: 99%

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Type I IFNs Stimulate Nitric Oxide Production and Resistance to Trypanosoma cruzi Infection

Costa

Torres

Mendonça

et al. 2006

The Journal of Immunology

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The participation of type I IFNs (IFN-I) in NO production and resistance to Trypanosoma cruzi infection was investigated. Adherent cells obtained from the peritoneal cavity of mice infected by the i.p. route produced NO and IFN-I. Synthesis of NO by these cells was partially inhibited by treatment with anti-IFN-αβ or anti-TNF-α Abs. Compared with susceptible BALB/c mice, peritoneal cells from parasite-infected resistant C57BL/6 mice produced more NO (2-fold), IFN-I (10-fold), and TNF-α (3.5-fold). Later in the infection, IFN-I levels measured in spleen cell (SC) cultures from 8-day infected mice were greater in C57BL/6 than in infected BALB/c mice, and treatment of the cultures with anti-IFN-αβ Ab reduced NO production. IFN-γ or IL-10 production by SCs was not different between the two mouse strains; IL-4 was not detectable. Treatment of C57BL/6 mice with IFN-I reduced parasitemia levels in the acute phase of infection. Mice deprived of the IFN-αβR gene developed 3-fold higher parasitemia levels in the acute phase in comparison with control 129Sv mice. Production of NO by peritoneal macrophages and SCs was reduced in mice that lacked signaling by IFN-αβ, whereas parasitism of macrophages was heavier than in control wild-type mice. We conclude that IFN-I costimulate NO synthesis early in T. cruzi infection, which contributes to a better control of the parasitemia in resistant mice.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Type I IFNs Stimulate Nitric Oxide Production and Resistance to Trypanosoma cruzi Infection

Costa

Torres

Mendonça

et al. 2006

The Journal of Immunology

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“…IL-10 is known to exert an important anti-inflammatory effect, inhibiting the synthesis of nitrite by macrophages and the production of IFN-γ by CD4 + T lymphocytes. The effects of this cytokine include the inhibition of a protective immune response and escape of the parasite, thus contributing to the establishment of infection 16,29,30 . The significant increase in the production of IL-10 by whole blood cells after addition of the parasite to the culture suggests that this cytokine indeed contributes to parasite escape.…”

Section: Conflict Of Interest Financial Support Referencesmentioning

confidence: 99%

Production of cytokine and chemokines by human mononuclear cells and whole blood cells after infection with Trypanosoma cruzi

Rezende-Oliveira

Sarmento

Rodrigues

2012

Rev. Soc. Bras. Med. Trop.

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INTRODUCTION: The innate immune response is the first mechanism of protection against Trypanosoma cruzi, and the interaction of inflammatory cells with parasite molecules may activate this response and modulate the adaptive immune system. This study aimed to analyze the levels of cytokines and chemokines synthesized by the whole blood cells (WBC) and peripheral blood mononuclear cells (PBMC) of individuals seronegative for Chagas disease after interaction with live T. cruzi trypomastigotes. METHODS: IL-12, IL-10, TNF-α, TGF-β, CCL-5, CCL-2, CCL-3, and CXCL-9 were measured by ELISA. Nitrite was determined by the Griess method. RESULTS: IL-10 was produced at high levels by WBC compared with PBMC, even after incubation with live trypomastigotes. Production of TNF-α by both PBMC and WBC was significantly higher after stimulation with trypomastigotes. Only PBMC produced significantly higher levels of IL-12 after parasite stimulation. Stimulation of cultures with trypomastigotes induced an increase of CXCL-9 levels produced by WBC. Nitrite levels produced by PBMC increased after the addition of parasites to the culture. CONCLUSIONS: Surface molecules of T. cruzi may induce the production of cytokines and chemokines by cells of the innate immune system through the activation of specific receptors not evaluated in this experiment. The ability to induce IL-12 and TNF-α contributes to shift the adaptive response towards a Th1 profile.

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“…The protective immune responses elicited by T. cruzi are also associated with IFN-␥ (18,19) and TNF-␣ (20,21) and the control of tissue parasitism appears to be dependent on the generation of reactive nitrogen intermediates by the inducible NO synthase (22)(23)(24). Furthermore, endogenous IFN-␥ has been shown to play an important role in promoting recruitment of T lymphocytes and inflammation in the heart tissue from infected mice (13,14,25).…”

Section: O Ne Of the Hallmarks Of Infection With Trypanosoma Cruzimentioning

confidence: 99%

Intercellular Adhesion Molecule 1 Deficiency Leads to Impaired Recruitment of T Lymphocytes and Enhanced Host Susceptibility to Infection withTrypanosoma cruzi

Michailowsky

Celes

Marino

et al. 2004

The Journal of Immunology

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In this study, we investigated the involvement of Th1 cytokines in the expression of cell adhesion molecules (CAM) and recruitment of inflammatory cells to the heart of mice infected with Trypanosoma cruzi. Our results show that endogenously produced IFN-γ is essential to induce optimal expression of VCAM-1 and ICAM-1 on the cardiac vascular endothelium of infected mice. Furthermore, the influx of inflammatory cells into the cardiac tissue was impaired in Th1 cytokine-deficient infected mice, paralleling the intensity of VCAM-1 and ICAM-1 expression on the vascular endothelium. Consistent with the importance of ICAM-1 in host resistance, ICAM-1 knockout (KO) mice were highly susceptible to T. cruzi infection, as assessed by mortality rate, parasitemia, and heart tissue parasitism. The enhanced parasitism was associated with a decrease in the numbers of CD4+ and CD8+ T lymphocytes in the heart tissue of ICAM-1 KO mice. Additionally, ICAM-1 KO mice mounted an unimpaired IFN-γ response and IFN-γ-dependent production of reactive nitrogen intermediates and parasite- specific IgG2a. Supporting the participation of ICAM-1 in cell migration during T. cruzi infection, the entrance of adoptively transferred PBL from T. cruzi-infected wild-type C57BL/6 mice into the cardiac tissue of ICAM-1 KO mice was significantly abrogated. Therefore, we favor the hypothesis that ICAM-1 plays a crucial role in T lymphocyte recruitment to the cardiac tissue and host susceptibility during T. cruzi infection.

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Trypanosoma cruzi:IL-10, TNF, IFN-γ, and IL-12 Regulate Innate and Acquired Immunity to Infection

Cited by 174 publications

References 0 publications

Type I IFNs Stimulate Nitric Oxide Production and Resistance to Trypanosoma cruzi Infection

Type I IFNs Stimulate Nitric Oxide Production and Resistance to Trypanosoma cruzi Infection

Production of cytokine and chemokines by human mononuclear cells and whole blood cells after infection with Trypanosoma cruzi

Intercellular Adhesion Molecule 1 Deficiency Leads to Impaired Recruitment of T Lymphocytes and Enhanced Host Susceptibility to Infection withTrypanosoma cruzi

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