Interleukin‐10 and tumour necrosis factor‐alpha serum levels in chronic Chagas disease patients

Vasconcelos, Romero Henrique Teixeira; Azevedo, Elisa de Almeida Neves; Diniz, George Tadeu Nunes; Cavalcanti, Maria da Glória Aureliano de Melo; Oliveira, Wilson de; Morais, Clarice Neuenschwander Lins de; Gomes, Yara de Miranda

doi:10.1111/pim.12183

Cited by 19 publications

(13 citation statements)

References 17 publications

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“…Moderate physical training improved the response to infection, decreased the parasite peak, and increased survival in mice that were infected with T. cruzi [9]. IL-10 is important in regulating the immune response, inflammatory response, and tissue damage, through its ability to "turn off" the production of inflammatory cytokines by T lymphocytes [21]. In the present study, serum IL-10 levels were elevated in the CHD group.…”

Section: Discussionsupporting

confidence: 48%

“…In the present study, serum IL-10 levels were elevated in the CHD group. Elevations of this cytokine were also observed in asymptomatic patients, suggesting that IL-10 is part of a regulated immune response in patients without cardiomyopathy [21], and the presence of this cytokine is indicative of a good prognosis. Exogenous supplementation with IL-10 in Chagas disease can be useful for controlling myocarditis [22], in addition to controlling cardiac fibrosis.…”

Section: Discussionmentioning

confidence: 90%

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Physical training improves cardiopulmonary functional capacity and increases cytokine IL-10 levels in individuals with Chagas disease

Lopes¹,

Ferreira²,

Silva³

et al. 2017

Trop. J. Pharm Res

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Section: Discussionsupporting

confidence: 48%

Section: Discussionmentioning

confidence: 90%

Physical training improves cardiopulmonary functional capacity and increases cytokine IL-10 levels in individuals with Chagas disease

Lopes¹,

Ferreira²,

Silva³

et al. 2017

Trop. J. Pharm Res

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“…Its protective role has been assigned to the amplification of NO production ( 48 – 50 ) and to the induction of a germinal center response with generation of specific Abs for T. cruzi ( 51 ). Despite its well-established role in protection during T. cruzi infection, TNF has also been described as a mediator of immunopathology ( 33 , 52 ). We determined that high levels of plasma TNF in T. cruzi -infected muMT mice were associated with increased liver pathology, decreased body weight, increased liver transaminases, altered kinetic of plasma glucose, and high mortality.…”

Section: Discussionmentioning

confidence: 99%

Unconventional Pro-inflammatory CD4+ T Cell Response in B Cell-Deficient Mice Infected with Trypanosoma cruzi

et al. 2017

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Chagas disease, caused by the parasite Trypanosoma cruzi, is endemic in Latin America but has become a global public health concern by migration of infected people. It has been reported that parasite persistence as well as the intensity of the inflammatory immune response are determinants of the clinical manifestations of the disease. Even though inflammation is indispensable for host defense, when deregulated, it can contribute to tissue injury and organ dysfunction. Here, we report the importance of B cells in conditioning T cell response in T. cruzi infection. Mice deficient in mature B cells (muMT mice) infected with T. cruzi exhibited an increase in plasma TNF concentration, TNF-producing CD4+ T cells, and mortality. The increase in TNF-producing CD4+ T cells was accompanied by a reduction in IFNγ+CD4+ T cells and a decrease of the frequency of regulatory Foxp3+, IL-10+, and IL17+CD4+ T cells populations. The CD4+ T cell population activated by T. cruzi infection, in absence of mature B cells, had a high frequency of Ly6C+ cells and showed a lower expression of inhibitory molecules such as CTLA-4, PD-1, and LAG3. CD4+ T cells from infected muMT mice presented a high frequency of CD62LhiCD44− cells, which is commonly associated with a naïve phenotype. Through transfer experiments we demonstrated that CD4+ T cells from infected muMT mice were able to condition the CD4+ T cells response from infected wild-type mice. Interestingly, using Blimp-flox/flox-CD23icre mice we observed that in absence of plasmablast/plasma cell T. cruzi-infected mice exhibited a higher number of TNF-producing CD4+ T cells. Our results showed that the absence of B cells during T. cruzi infection affected the T cell response at different levels and generated a favorable scenario for unconventional activation of CD4+ T cell leading to an uncontrolled effector response and inflammation. The product of B cell differentiation, the plasmablast/plasma cells, could be able to regulate TNF-producing CD4+ T cells since their absence favor the increase of the number of TNF+ CD4+ in T. cruzi-infected mice.

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“…However, this critical cytokine is described to activate and coordinate, in part, the cardiac inflammatory response in the murine model of T. cruzi infection as well as in human Chagas disease [2, 4]. In this inflammatory context, the presence of inflammatory cytokines such as TNF and IFN-gamma is a trigger to different chemokines expression in the mononuclear and cardiac cells from animals infected with T. cruzi [35]. Chemokines are responsible for the recruitment of leukocytes into the infected tissue coordinating the magnificence of the inflammatory process.…”

Section: Discussionmentioning

confidence: 99%

Potential Role of Carvedilol in the Cardiac Immune Response Induced by Experimental Infection with Trypanosoma cruzi

Horta

Leite

Costa

et al. 2017

BioMed Research International

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Trypanosoma cruzi causes a cardiac infection characterized by an inflammatory imbalance that could become the inciting factor of the illness. To this end, we evaluated the role of carvedilol, a beta-blocker with potential immunomodulatory properties, on the immune response in C57BL/6 mice infected with VL-10 strain of T. cruzi in the acute phase. Animals (n = 40) were grouped: (i) not infected, (ii) infected, (iii) infected + carvedilol, and (iv) not infected + carvedilol. We analyzed parameters related to parasitemia, plasma levels of TNF, IL-10, and CCL2, and cardiac histopathology after the administration of carvedilol for 30 days. We did not observe differences in the maximum peaks of parasitemia in the day of their detection among the groups. The plasma TNF was elevated at 60 days of infection in mice treated or not with carvedilol. However, we observed a decreased CCL2 level and increased IL-10 levels in those infected animals treated with carvedilol, which impacted the reduction of the inflammatory infiltration in cardiac tissue. For this experimental model, carvedilol therapy was not able to alter the levels of circulating parasites but modulates the pattern of CCL2 and IL-10 mediators when the VL10 strain of T. cruzi was used in C57BL6 mice.

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Interleukin‐10 and tumour necrosis factor‐alpha serum levels in chronic Chagas disease patients

Cited by 19 publications

References 17 publications

Physical training improves cardiopulmonary functional capacity and increases cytokine IL-10 levels in individuals with Chagas disease

Physical training improves cardiopulmonary functional capacity and increases cytokine IL-10 levels in individuals with Chagas disease

Unconventional Pro-inflammatory CD4+ T Cell Response in B Cell-Deficient Mice Infected with Trypanosoma cruzi

Potential Role of Carvedilol in the Cardiac Immune Response Induced by Experimental Infection with Trypanosoma cruzi

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