Trypanosoma cruzi infection induces up-regulation of cardiac muscarinic acetylcholine receptors in vivo and in vitro

Peraza-Cruces, K.; Gutiérrez-Guédez, L.; Perozo, D. Castañeda; Lankford, C.R.; Rodríguez-Bonfante, Claudina; Bonfante-Cabarcas, Rafael

doi:10.1590/s0100-879x2008000900009

Cited by 13 publications

(8 citation statements)

References 33 publications

(39 reference statements)

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“…8 It is important to point out that there are other possible factors involved in altered electrical properties of right ventricular myocytes. Accordingly, T. cruzi infection increases expression of β-adrenergic 16 and muscarinic receptors, 34 which are known to modulate ionic currents in ventricular myocytes.…”

Section: Discussionmentioning

confidence: 99%

Altered Cardiomyocyte Function and Trypanosoma cruzi Persistence in Chagas Disease

Cruz¹,

Santos‐Miranda²,

Sales-Junior³

et al. 2016

The American Journal of Tropical Medicine and Hygiene

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Abstract. Chagas disease, caused by the triatominae Trypanosoma cruzi, is one of the leading causes of heart malfunctioning in Latin America. The cardiac phenotype is observed in 20-30% of infected people 10-40 years after their primary infection. The cardiac complications during Chagas disease range from cardiac arrhythmias to heart failure, with important involvement of the right ventricle. Interestingly, no studies have evaluated the electrical properties of right ventricle myocytes during Chagas disease and correlated them to parasite persistence. Taking advantage of a murine model of Chagas disease, we studied the histological and electrical properties of right ventricle in acute (30 days postinfection [dpi]) and chronic phases (90 dpi) of infected mice with the Colombian strain of T. cruzi and their correlation to parasite persistence. We observed an increase in collagen deposition and inflammatory infiltrate at both 30 and 90 dpi. Furthermore, using reverse transcriptase polymerase chain reaction, we detected parasites at 90 dpi in right and left ventricles. In addition, we observed action potential prolongation and reduced transient outward K + current and L-type Ca 2+ current at 30 and 90 dpi. Taking together, our results demonstrate that T. cruzi infection leads to important modifications in electrical properties associated with inflammatory infiltrate and parasite persistence in mice right ventricle, suggesting a causal role between inflammation, parasite persistence, and altered cardiomyocyte function in Chagas disease. Thus, arrhythmias observed in Chagas disease may be partially related to altered electrical function in right ventricle.

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Section: Discussionmentioning

confidence: 99%

Altered Cardiomyocyte Function and Trypanosoma cruzi Persistence in Chagas Disease

Cruz¹,

Santos‐Miranda²,

Sales-Junior³

et al. 2016

The American Journal of Tropical Medicine and Hygiene

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“…In relation to IL1β and cardiovascular disease, Testa et al 36 reported that 25 to 37% of HF patients due to coronary heart disease and/or hypertension, ranging from NYHA class III to NYHA class IV, displayed higher levels of IL1β, which was correlated with severity of the disease. Similarly, Peraza-Cruces et al 37 showed that IL1β levels were elevated in the plasma of rats with chronic Chagas disease and in an in vitro Chagas disease model conditioned medium.…”

Section: Discussionmentioning

confidence: 87%

Prevalence of Trypanosoma cruzi antibodies and inflammatory markers in uncompensated heart failure

Bravo-Tobar

Parra²,

Pérez

et al. 2011

Rev. Soc. Bras. Med. Trop.

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Introduction: Heart failure (HF) represents the final stage of chronic chagasic cardiomyopathy (CChC). The diagnosis of CChC is based on the demonstration of anti-Trypanosoma cruzi antibodies (aTcAg) and clinical and epidemiological data. In Venezuela, there are no data about the prevalence of chagasic HF. The aim of this study was to determine the epidemiological, clinical, and inflammatory risk factors associated with seronegative or seropositive HF patients. Methods: We performed a cross-sectional study in the Venezuelan central-west states among a healthy rural population and in patients admitted to the emergency room with uncompensated HF. Results: The seroprevalence rates of Trypanosoma cruzi antibodies were 11.2% and 40.1% in the healthy population and in HF patients, respectively. Seropositivity in healthy individuals was associated with age, knowledge on triatomine vectors, and having seen wild reservoirs in the house; in HF patients, with contact with the vector and previous clinical diagnosis of Chagas' disease; and in both groups taken together, with age, knowledge on triatomines, and HF. Seropositive patients had prolonged QRS, decreased ejection fraction, and high serum magnesium, all significant as compared with HF seronegative cases. Left atrium enlargement and ventricular hypertrophy were most frequently observed in HF seronegative patients. CRP, IL6, ILβ1, IL2, and FNTα were elevated in 94.5%, 48%, 17.8%, 13.7%, and 6.9% of HF patients, respectively, but only IL2 levels were associated with chagasic HF. Conclusions: There is a high prevalence of aTcAg in HF patients from the central-west region of Venezuela, and their epidemiological, clinical, and inflammatory features are discreetly different as compared with those of seronegative cases.

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“…Our results demonstrate that muscarinic receptors were up-regulated in the right ventricular myocardium and peripheral blood mononuclear cells (PBMC) in rats suffering from chronic chagasic myocarditis, and in fetal cardiomyocyte co-culture with T. cruzi/PBMC in non contact fashion or treated with a conditioned medium obtained from T. cruzi-PBMC co-culture [14]. In a different publication, we observed that rats with chronic Chagas disease had parasympathetic disturbances that could be the consequence of alterations on the muscarinic receptor distribution at different neural integration levels [15].…”

Section: Introductionmentioning

confidence: 74%

“…We have previously studied muscarinic cholinergic receptors through in vivo and in vitro models of Chagas' disease [14] [15]. Our results demonstrate that muscarinic receptors were up-regulated in the right ventricular myocardium and peripheral blood mononuclear cells (PBMC) in rats suffering from chronic chagasic myocarditis, and in fetal cardiomyocyte co-culture with T. cruzi/PBMC in non contact fashion or treated with a conditioned medium obtained from T. cruzi-PBMC co-culture [14].…”

Section: Introductionmentioning

confidence: 79%

A Decreased Expression and Functionality of Muscarinic Cholinergic Receptor in Acute Chagas Myocarditis

Labrador-Hernández¹,

Jimenez²,

León³

et al. 2014

WJCD

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Background: Chagas disease is still a public health problem because of the remaining high prevalence, the expansion of the disease into developed countries and the re-emergences by oral transmission outbreaks. Chagas cardiomyopathy evolves as a consequence of an autonomic unbalance where the parasympathetic tone is undermined. Objective: To determine the functionality and expression of muscarinic cholinergic receptors in acute Chagas disease. Methodology: 62 male, 3-week-old Sprague Dawley rats were assayed; 32 were infected with Trypanosoma cruzi trypomastigotes and 30 were healthy controls. Electrocardiographic studies were conducted in the absence or presence of direct muscarinic (oxotremorine and McN-A-343) or indirect agonists (phenylephrine) or antagonist (pirenzepine). Muscarinic M1 and M2 receptor expression was determined by radioligand [ 3 H]-QNB binding assay and immunoblot. Results: Chagasic acute myocarditis was sustained by electrocardiographic signs and histopathological findings. Bradycardia induced by oxotremorine was significantly higher in healthy rats (HR) and the differences were enhanced by CsCl. In the absence of the agonist, CsCl induced a greater bradycardia in chagasic rats (ChR). In HR McN-A-343 induced tachycardia, however it induces bradycardia in the presence of a acetylcholinesterase inhibitor (neostigmine); no effects were observed in ChR. Pirenzepine induced a higher tachycardia in HR. Phenylephrine in the presence of pirenzepine induced a similar bradycardia in both groups, but recovery was faster in ChR. Muscarinic M1 and M2 receptor density was higher in HR. Conclusion: Muscarinic receptor expression and functionality are decreased * Corresponding author. M. Labrador-Hernández et al. 306in the acute Chagas disease that could impact the evolution and prognosis of the disease.

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Trypanosoma cruzi infection induces up-regulation of cardiac muscarinic acetylcholine receptors in vivo and in vitro

Cited by 13 publications

References 33 publications

Altered Cardiomyocyte Function and Trypanosoma cruzi Persistence in Chagas Disease

Altered Cardiomyocyte Function and Trypanosoma cruzi Persistence in Chagas Disease

Prevalence of Trypanosoma cruzi antibodies and inflammatory markers in uncompensated heart failure

A Decreased Expression and Functionality of Muscarinic Cholinergic Receptor in Acute Chagas Myocarditis

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