Faculty Opinions recommendation of Doxycycline and Benznidazole Reduce the Profile of Th1, Th2, and Th17 Chemokines and Chemokine Receptors in Cardiac Tissue from Chronic Trypanosoma cruzi-Infected Dogs.

2016 ◽  
Author(s):  
Herbert Tanowitz ◽  
Fabiana Machado
Keyword(s):  
Trypanosoma Cruzi ◽  
Chemokine Receptors ◽  
Cardiac Tissue

scholarly journals Doxycycline and Benznidazole Reduce the Profile of Th1, Th2, and Th17 Chemokines and Chemokine Receptors in Cardiac Tissue from ChronicTrypanosoma cruzi-Infected Dogs

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Guilherme de Paula Costa ◽  
Laís Roquete Lopes ◽  
Maria Cláudia da Silva ◽  
Aline Luciano Horta ◽  
Washington Martins Pontes ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Chemokine Receptors ◽  
Cardiac Tissue ◽  
Chronic Phase ◽  
Term Treatment ◽  
Cardiac Protection ◽  
Ccr5 Expression ◽  
Qpcr Analysis ◽  
Long Term Treatment

Chemokines (CKs) and chemokine receptors (CKR) promote leukocyte recruitment into cardiac tissue infected by theTrypanosoma cruzi. This study investigated the long-term treatment with subantimicrobial doses of doxycycline (Dox) in association, or not, with benznidazole (Bz) on the expression of CK and CKR in cardiac tissue. Thirty mongrel dogs were infected, or not, with the Berenice-78 strain ofT. cruziand grouped according their treatments: (i) two months after infection, Dox (50 mg/kg) 2x/day for 12 months; (ii) nine months after infection, Bz (3,5 mg/kg) 2x/day for 60 days; (iii) Dox + Bz; and (iv) vehicle. After 14 months of infection, hearts were excised and processed for qPCR analysis of Th1 (CCL2, CCL3, CCL4, CCL5, CXCL9, and CXCL11), Th2 (CCL1, CCL17, CCL24, and CCL26), Th17 (CCL20) CKs, Th1 (CCR5, CCR6, and CXCR3), and Th2/Th17 (CCR3, CCR4, and CCR8) CKR, as well as IL-17.T. cruziinfection increases CCL1, CCL2, CCL4, CCL5, CCL17, CXCL10, and CCR5 expression in the heart. Dox, Bz, or Dox + Bz treatments cause a reversal of CK and CKR and reduce the expression of CCL20, IL-17, CCR6, and CXCR3. Our data reveal an immune modulatory effect of Dox with Bz, during the chronic phase of infection suggesting a promising therapy for cardiac protection.

Dynamics of T Cells Repertoire During Trypanosoma cruzi Infection and its Post-Treatment Modulation

2019 ◽  
Vol 26 (36) ◽  
pp. 6519-6543 ◽  
Author(s):  
Adriana Egui ◽  
Paola Lasso ◽  
Elena Pérez-Antón ◽  
M. Carmen Thomas ◽  
Manuel Carlos López
Keyword(s):  
Immune Response ◽  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Cardiac Tissue ◽  
Acute Infection ◽  
Clinical Status ◽  
Chronic Phase ◽  
Parasite Load ◽  
Chronic Patients ◽  
Cruzi Infection

Chagas disease courses with different clinical phases and has a variable clinical presentation and progression. The acute infection phase mostly exhibits a non-specific symptomatology. In the absence of treatment, the acute phase is followed by a chronic phase, which is initially asymptomatic. This chronic asymptomatic phase of the disease is characterized by a fragile balance between the host’s immune response and the parasite replication. The loss of this balance is crucial for the progression of the sickness. The virulence and tropism of the T. cruzi infecting strain together to the inflammation processes in the cardiac tissue are the main factors for the establishment and severity of the cardiomyopathy. The efficacy of treatment in chronic Chagas disease patients is controversial. However, several studies carried out in chronic patients demonstrated that antiparasitic treatment reduces parasite load in the bloodstream and leads to an improvement in the immune response against the Trypanosoma cruzi parasite. The present review is mainly focused on the cellular patterns associated to the clinical status and the evolution of the disease in chronic patients, as well as the effectiveness of the treatment related to T. cruzi infection control. Therefore, an emphasis is placed on the dynamics of specific-antigens T cell subpopulations, their memory and activation phenotypes, their functionality and their contribution to pathogenesis or disease control, as well as their association with risk of congenital transmission of the parasite.

scholarly journals Trypanosoma cruzi: Effect of the absence of 5-lipoxygenase (5-LO)-derived leukotrienes on levels of cytokines, nitric oxide and iNOS expression in cardiac tissue in the acute phase of infection in mice

2011 ◽  
Vol 127 (1) ◽  
pp. 58-65 ◽  
Author(s):  
Carolina Panis ◽  
Tânia Longo Mazzuco ◽  
Cauê Zortéa Fernandes Costa ◽  
Vanessa Jacob Victorino ◽  
Vera Lúcia Hideko Tatakihara ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Trypanosoma Cruzi ◽  
Acute Phase ◽  
Cardiac Tissue ◽  
Inos Expression

scholarly journals Chronic Trypanosoma cruzi-elicited cardiomyopathy: from the discovery to the proposal of rational therapeutic interventions targeting cell adhesion molecules and chemokine receptors - how to make a dream come true

2009 ◽  
Vol 104 (suppl 1) ◽  
pp. 226-235 ◽  
Author(s):  
Joseli Lannes-Vieira ◽  
Jaline Coutinho Silverio ◽  
Isabela Resende Pereira ◽  
Nathália Ferreira Vinagre ◽  
Cristiano Marcelo Espinola Carvalho ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Trypanosoma Cruzi ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Chemokine Receptors ◽  
Therapeutic Interventions

Melatonin decreases circulating Trypanosoma cruzi load with no effect on tissue parasite replication.

2020 ◽  
Author(s):  
MAIARA VOLTARELLI PROVIDELLO ◽  
Gisele Bulhões Portapilla ◽  
Pedro Alexandre Sampaio Oliveira ◽  
Carla Brigagão Pacheco da Silva ◽  
Naira Ferreira Anchieta ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Cardiac Tissue ◽  
Direct Action ◽  
Protective Action ◽  
Cardiac Damage ◽  
Redox Imbalance ◽  
Parasitic Load ◽  
Parasite Replication

Cardiac damage during the acute phase of Chagas disease (CD) is associated with an increase in pro-inflammatory markers and oxidative stress. Melatonin has emerged as a promising therapy for CD due to its antioxidant and immunomodulatory properties. However, the protective action of melatonin in the cardiac tissue as well as its direct action on the parasite cycle is not fully understood. We investigated the effects of melatonin on heart parasitism in mice infected with Trypanosoma cruzi (T. cruzi) and also its effects on the parasitic proliferation in vitro. Our in vivo study showed that melatonin reduced circulating parasitemia load, but did not control tissue (heart, liver and spleen) parasitism in mice. Melatonin did not prevent the redox imbalance in the left ventricle of infected mice. Our in vitro findings showed that melatonin did not inhibit parasites replication within cells, but rather increased their release from cells. Melatonin did not control parasitism load in the heart or prevented the cardiac redox imbalance induced by acute T. cruzi infection. The hormone controlled the circulating parasitic load, but in cells melatonin accelerated parasitic release, a response that can be harmful.

Detection of Trypanosoma cruzi with the Polymerase Chain Reaction and in Situ Hybridization in Infected Murine Cardiac Tissue

1997 ◽  
Vol 56 (6) ◽  
pp. 588-595 ◽  
Author(s):  
Joshua E. Lane ◽  
Clint E. Carter ◽  
Thomas L. McCurley ◽  
Cindy L. Vnencak-Jones ◽  
Danyvid Olivares-Villagomez
Keyword(s):  
Polymerase Chain Reaction ◽  
In Situ Hybridization ◽  
Trypanosoma Cruzi ◽  
Cardiac Tissue ◽  
Chain Reaction ◽  
Polymerase Chain

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

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Aline Luciano Horta ◽  
Ana Luisa Junqueira Leite ◽  
G. Paula Costa ◽  
Vivian Paulino Figueiredo ◽  
André Talvani
Keyword(s):  
Immune Response ◽  
Trypanosoma Cruzi ◽  
Experimental Infection ◽  
Potential Role ◽  
Cardiac Tissue ◽  
Inflammatory Infiltration ◽  
Ccl2 Level ◽  
Immunomodulatory Properties ◽  
Cardiac Histopathology

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.

scholarly journals Glutamine increases body weight and decreases myocardial damage in Trypanosoma cruzi-infected mice treated with nifurtimox.

2021 ◽  
Vol 23 (1) ◽  
pp. 10-16
Author(s):  
Carmen Marín-Tello ◽  
◽  
César Sánchez-Marín ◽  
Luis Arteaga-Temoche ◽  
◽  
...  
Keyword(s):  
Body Weight ◽  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Rural Areas ◽  
Cardiac Tissue ◽  
Parasitic Infection ◽  
Myocardial Damage ◽  
Glutamine Supplementation ◽  
Histopathological Analysis ◽  
Standard Diet

Chagas disease, a parasitic infection caused by the protist Trypanosoma cruzi, affect the poorest populations, living in remote, rural areas and urban slums. Although this drug is effective against Chagas disease present a number of serious side effects. In residents of high Andean areas with megacolon it can lead to cardiomyopathies. The aim of this study was to investigate whether dietary supplementation with L-glutamine may alleviate some of these symptoms because of its previously observed anti-inflammatory properties. We studied two groups of T. cruzi-infected mice receiving treatment with nifurtimox. One group was fed the standard diet, while the other group’s diet was supplemented with Glutamine. We found that Glutamine supplementation increases body weight (p<0.001), decreases heart mass to body mass ratio (p<0.001), and decreases the number of amastigotes present in cardiac tissue. Additionally, histopathological analysis showed less heart tissue damage in the group that received Glutaminne in their diet. Therefore, our findings suggest that Glutamine supplementation improves nifurtimox treatment outcomes of T. cruzi infection.

scholarly journals The CC Chemokine Receptor 5 Is Important in Control of Parasite Replication and Acute Cardiac Inflammation following Infection with Trypanosoma cruzi

2006 ◽  
Vol 74 (1) ◽  
pp. 135-143 ◽  
Author(s):  
Jenny L. Hardison ◽  
Ruth A. Wrightsman ◽  
Philip M. Carpenter ◽  
William A. Kuziel ◽  
Thomas E. Lane ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Chemokine Receptor ◽  
Chemokine Receptors ◽  
Acute Infection ◽  
Parasite Burden ◽  
Chronic Inflammatory Response ◽  
Cc Chemokine ◽  
Parasite Replication ◽  
Cc Chemokine Receptor 5 ◽  
Chemokine Receptor 5

ABSTRACT Infection of susceptible mice with the Colombiana strain of Trypanosoma cruzi results in an orchestrated expression of chemokines and chemokine receptors within the heart that coincides with parasite burden and cellular infiltration. CC chemokine receptor 5 (CCR5) is prominently expressed during both acute and chronic disease, suggesting a role in regulating leukocyte trafficking and accumulation within the heart following T. cruzi infection. To better understand the functional role of CCR5 and its ligands with regard to both host defense and/or disease, CCR5−/− mice were infected with T. cruzi, and the disease severity was evaluated. Infected CCR5−/− mice develop significantly higher levels of parasitemia (P ≤ 0.05) and cardiac parasitism (P ≤ 0.01) during acute infection that correlated with reduced survival. Further, we show that CCR5 is essential for directing the migration of macrophages and T cells to the heart early in acute infection with T. cruzi. In addition, data are provided demonstrating that CCR5 does not play an essential role in maintaining inflammation in the heart during chronic infection. Collectively, these studies clearly demonstrate that CCR5 contributes to the control of parasite replication and the development of a protective immune response during acute infection but does not ultimately participate in maintaining a chronic inflammatory response within the heart.

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