Cytokines in innate and acquired immunity to Trypanosoma cruzi infection

Abrahamsohn, Ises A.

doi:10.1590/s0100-879x1998000100015

Cited by 48 publications

(36 citation statements)

References 38 publications

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“…Experimental investigations of immunologic responses during acute infection have preferentially been developed in the mice model (Silva et al 1991, Abrahamsohn 1998 which contributes to clarify the pathogenesis of lesions. In the murine model, infection with T. cruzi is followed by activation of macrophages as an initial innate response, mediated by IFN-γ produced by natural killer cells (Cardillo et al 1996).…”

Section: Discussionmentioning

confidence: 99%

Participation of cytokines in the necrotic-inflammatory lesions in the heart and skeletal muscles of Calomys callosus infected with Trypanosoma cruzi

Magalhães-Santos

Andrade

2005

Mem. Inst. Oswaldo Cruz

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Section: Discussionmentioning

confidence: 99%

Participation of cytokines in the necrotic-inflammatory lesions in the heart and skeletal muscles of Calomys callosus infected with Trypanosoma cruzi

Magalhães-Santos

Andrade

2005

Mem. Inst. Oswaldo Cruz

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“…The parasite was able to stimulate the synthesis of proinflammatory (TNF-α) and anti-inflammatory mediators (IL-10 and TGF-β) that are responsible for the modulation of nitrite synthesis, with consequent effects on trypanocidal capacity 26,27 . The significant production of IL-12 and TNF-α highlights the importance of these two cytokines during the early stages of infection, with IL-12 inducing the differentiation of Th1 lymphocytes and TNF-α activating iNOS.…”

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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“…Indeed, it has been shown that damaged ECM activates macrophages to secrete IL-12 and chemokines (37,38), cytokines present in the inflamed heart of chronic chagasic patients (24,25), and in acute and chronic experimentally T. cruzi-infected mice (23,39,40). These cytokines play a central role by controlling tissue parasitism during T. cruzi infection but are also involved in the maintenance of chronic myocarditis (41)(42)(43)(44).…”

Section: The Host Answersmentioning

confidence: 99%

Trypanosoma cruzi infection: a continuous invader-host cell cross talk with participation of extracellular matrix and adhesion and chemoattractant molecules

Marino¹,

Silva²,

Pinho

et al. 2003

Braz J Med Biol Res

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Several lines of evidence have shown that Trypanosoma cruzi interacts with host extracellular matrix (ECM) components producing breakdown products that play an important role in parasite mobilization and infectivity. Parasite-released antigens also modulate ECM expression that could participate in cell-cell and/or cell-parasite interactions. Increased expression of ECM components has been described in the cardiac tissue of chronic chagasic patients and diverse target tissues including heart, thymus, central nervous system and skeletal muscle of experimentally T. cruzi-infected mice. ECM components may adsorb parasite antigens and cytokines that could contribute to the establishment and perpetuation of inflammation. Furthermore, T. cruzi-infected mammalian cells produce cytokines and chemokines that not only participate in the control of parasitism but also contribute to the establishment of chronic inflammatory lesions in several target tissues and most frequently lead to severe myocarditis. T. cruzi-driven cytokines and chemokines may also modulate VCAM-1 and ICAM-1 adhesion molecules on endothelial cells of target tissues and play a key role in cell recruitment, especially of activated VLA-4 + LFA-1 + CD8 + T lymphocytes, resulting in a predominance of this cell population in the inflamed heart, central nervous system and skeletal muscle. The VLA-4 + -invading cells are surrounded by a fine network of fibronectin that could contribute to cell anchorage, activation and effector functions. Since persistent "danger signals" triggered by the parasite and its antigens are required for the establishment of inflammation and ECM alterations, therapeutic interventions that control parasitism and selectively modulate cell migration improve ECM abnormalities, paving the way for the development of new therapeutic strategies improving the prognosis of T. cruzi-infected individuals.

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Cytokines in innate and acquired immunity to Trypanosoma cruzi infection

Cited by 48 publications

References 38 publications

Participation of cytokines in the necrotic-inflammatory lesions in the heart and skeletal muscles of Calomys callosus infected with Trypanosoma cruzi

Participation of cytokines in the necrotic-inflammatory lesions in the heart and skeletal muscles of Calomys callosus infected with Trypanosoma cruzi

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

Trypanosoma cruzi infection: a continuous invader-host cell cross talk with participation of extracellular matrix and adhesion and chemoattractant molecules

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