Immunoneuroendocrine alterations in patients with progressive forms of chronic Chagas disease

Pérez, Ana Rosa; Silva-Barbosa, Suse Dayse; Berbert, Luiz Ricardo; Revelli, Silvia; Beloscar, Juan; Savino, Wilson; Bottasso, Óscar

doi:10.1016/j.jneuroim.2011.03.010

Cited by 56 publications

(83 citation statements)

References 48 publications

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“…However, there was no significant effect of protection after the exclusion of the HLA Haplotype (Table 3). This result is consistent with an immunoendocrine analysis in patients with progressive forms of Chronic Chagas disease where they observed normal cortisol levels among the studied groups (Healthy, Indeterminate, Mild to moderate cardiac, and Severe cardiac); whereas a progressive diminution of DHEA-s levels, the sulfate ester of DHEA, was found as Chagas disease severity progressed in a previous study [3]. Furthermore, the DHEA and testosterone therapy in T. cruzi infected rats, improved the effectiveness of the host's immune response [16].…”

Section: Discussionsupporting

confidence: 91%

21-Hydroxylase gene mutant allele CYP21A2∗15 strongly linked to the resistant HLA haplotype B∗14:02-DRB1∗01:02 in chronic Chagas disease

Puerto¹,

Kikuchi

Nishizawa

et al. 2013

Human Immunology

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Section: Discussionsupporting

confidence: 91%

21-Hydroxylase gene mutant allele CYP21A2∗15 strongly linked to the resistant HLA haplotype B∗14:02-DRB1∗01:02 in chronic Chagas disease

Puerto¹,

Kikuchi

Nishizawa

et al. 2013

Human Immunology

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“…23 This was recently confirmed in a study measuring circulating TGF-β in 43 Argentinean patients. 24 It extended the idea that TGF-β and interleukin (IL)-6 are the cytokines that significantly differ between cardiac patients at different stages of heart disease progression. Other cytokines (tumor necrosis factor-α, IL-4, IL-17, interferon-γ, CCL2, and IL-10) showed differences between severe heart disease and the indeterminate stage but not among the different stages of heart disease progression.…”

Section: Tgf-β Levelsmentioning

confidence: 97%

The TGF-β Pathway as an Emerging Target for Chagas Disease Therapy

Bailly

et al. 2012

Clin Pharmacol Ther

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Transforming growth factor-β (TGF-β) influences the development of myocardiopathy in Chagas disease through regulation of (i) parasite invasion of heart cells, (ii) an intracellular parasite cycle, (iii) inflammation and immune response, (iv) heart fibrosis and remodeling, and (v) gap junction modulation and heart conduction. In this review, we discuss the rationale for developing TGF-β signaling-interfering therapies as adjuvant approaches for the management of the cardiac alterations of Chagas disease-affected patients.

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“…In this regard, a previous study carried out in a small group of urbanized patients with chronic Chagas' disease, showed that the more severe forms of myocarditis coexisted with immune-endocrine imbalances and a trend to overweight [12]. Coincidentally, another study detected a higher prevalence of diabetes in chagasic women with chronic myocarditis than in the general population [13].…”

Section: Introductionmentioning

confidence: 97%

“…For instance, unbalanced adipocytokines were associated with the presence of sympathetic dysfunctions in patients with CCC [21]. Moreover, cortisol/DHEA ratios, rather than the individual concentrations seem to be more representative of disease activity [11,12].…”

Section: Introductionmentioning

confidence: 99%

Dysregulated Network of Immune, Endocrine and Metabolic Markers is Associated to More Severe Human Chronic Chagas Cardiomyopathy

González

Villar

D’Attilio

et al. 2018

Neuroimmunomodulation

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Individuals who are infected with Trypanosoma cruzi develop chronic Chagas cardiomyopathy (CCC), which is a complication involving a series of immune pathogenetic mechanisms, although an association between immune and metabolic alterations was more recently proposed. Accordingly, we investigated the immuno-metabolic response in chagasic patients and their possible influence on CCC pathogenesis. To this end, T. cruzi-seropositive (asymptomatic or with CCC) and sero-negative individuals were studied. Serum tumour necrosis factor (TNF)-α, interleukin (IL)-6, adipocytokines and the expression of their receptors in peripheral blood mononuclear cell (PBMC) were evaluated, together with other factors influencing the immune response. CCC patients showed major metabolic and hormonal abnormalities, in parallel with increased IL-6 and leptin serum levels. TNF-α receptor s, leptin and adiponectin receptors (ObR and Adipo-Rs respectively), as well as PPAR-γ expression in PBMCs from CCC patients were compatible with a counteracting response leading to an unfavourable immune-metabolic profile. These results suggest that persistently increased levels of immune-metabolic pro-inflammatory mediators along with the adverse endocrine anti-inflammatory response of CCC individuals, may contribute to the underlying mechanisms dealing with myocardial tissue damage.

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Immunoneuroendocrine alterations in patients with progressive forms of chronic Chagas disease

Cited by 56 publications

References 48 publications

21-Hydroxylase gene mutant allele CYP21A2∗15 strongly linked to the resistant HLA haplotype B∗14:02-DRB1∗01:02 in chronic Chagas disease

21-Hydroxylase gene mutant allele CYP21A2∗15 strongly linked to the resistant HLA haplotype B∗14:02-DRB1∗01:02 in chronic Chagas disease

The TGF-β Pathway as an Emerging Target for Chagas Disease Therapy

Dysregulated Network of Immune, Endocrine and Metabolic Markers is Associated to More Severe Human Chronic Chagas Cardiomyopathy

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