Human acute Chagas disease: changes in factor VII, activated protein C and hepatic enzymes from patients of oral outbreaks in Pará State (Brazilian Amazon)

Santos, Valéria Regina Cavalcante dos; Antunes, Dina; Souza, Dilma do Socorro Moraes de; Moreira, Otacílio C.; Lima, Igor Campos de Almeida; Farias-de-Oliveira, Désio Aurélio; Lobo, João Pedro; Meis, Ernesto de; Coura, José Rodrigues; Savino, Wilson; Junqueira, Ângela Cristina Veríssimo; Meis, Juliana de

doi:10.1590/0074-02760190364

Cited by 8 publications

(8 citation statements)

References 23 publications

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“…(6,148) Another aspect to consider is that we are facing an acute infectious disease with chronic evolution of an inflammatory character in the acute phase, which suggests an alteration of coagulation factors, with thrombus and haemorrhage previously described. (143,149) In the pandemic scenario caused by Coronavirus disease 2019 (COVID-19), we warn of the possibility of coinfection at a time when there is no scientific evidence of the evolution of cases of coinfection of acute Chagas disease with other infectious diseases.…”

Section: Acute Chagas's Heart Disease: a New And Poorly Known Challengementioning

confidence: 99%

Prognosis of chronic Chagas heart disease and other pending clinical challenges

Torres

Correia

Nunes

et al. 2022

Mem. Inst. Oswaldo Cruz

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Section: Acute Chagas's Heart Disease: a New And Poorly Known Challengementioning

confidence: 99%

Prognosis of chronic Chagas heart disease and other pending clinical challenges

Torres

Correia

Nunes

et al. 2022

Mem. Inst. Oswaldo Cruz

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“…Today we know that the liver is important in the clearance of blood trypomastigote forms (4) and that the disease carries additional risk in patients with non-alcoholic steatohepatitis (NASH), as it exacerbates hepatic injury (5). Accordingly, acutely infected patients have very high levels of hepatic transaminases and activated C protein, with lower levels of coagulation factor VII (6). Although the infection of hepatocytes is not high as in the case of macrophages or cardiomyocytes in vivo, these results indicate the profound impact of the infection on this cell type.…”

Section: Introductionmentioning

confidence: 99%

In the Acute Phase of Trypanosoma cruzi Infection, Liver Lymphoid and Myeloid Cells Display an Ambiguous Phenotype Combining Pro- and Anti-Inflammatory Markers

et al. 2022

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Multiple cell populations, cellular biochemical pathways, and the autonomic nervous system contribute to maintaining the immunological tolerance in the liver. This tolerance is coherent because the organ is exposed to high levels of bacterial pathogen-associated molecular pattern (PAMP) molecules from the intestinal microbiota, such as lipopolysaccharide endotoxin (LPS). In the case of Trypanosoma cruzi infection, although there is a dramatic acute immune response in the liver, we observed intrahepatic cell populations combining pro- and anti-inflammatory markers. There was loss of fully mature Kupffer cells and an increase in other myeloid cells, which are likely to include monocytes. Among dendritic cells (DCs), the cDC1 population expanded relative to the others, and these cells lost both some macrophage markers (F4/80) and immunosuppressive cytokines (IL-10, TGF-β1). In parallel, a massive T cell response occured with loss of naïve cells and increase in several post-activation subsets. However, these activated T cells expressed both markers programmed cell death protein (PD-1) and cytokines consistent with immunosuppressive function (IL-10, TGF-β1). NK and NK-T cells broadly followed the pattern of T cell activation, while TCR-γδ cells appeared to be bystanders. While no data were obtained concerning IL-2, several cell populations also synthesized IFN-γ and TNF-α, which has been linked to host defense but also to tissue injury. It therefore appears that T. cruzi exerts control over liver immunity, causing T cell activation via cDC1 but subverting multiple populations of T cells into immunosuppressive pathways. In this way, T. cruzi engages a mechanism of hepatic T cell tolerance that is familiar from liver allograft tolerance, in which activation and proliferation are followed by T cell inactivation.

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“…In acute chagasic patients, most likely infected by the oral route, levels of hepatic transaminases and activated C protein were increased, although with lower levels of coagulation factor VII [ 61 ]. All these proteins are synthesized by hepatocytes and indicate the profound impact of the infection on this cell type.…”

Section: Introductionmentioning

confidence: 99%

The Liver and the Hepatic Immune Response in Trypanosoma cruzi Infection, a Historical and Updated View

et al. 2021

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Chagas disease was described more than a century ago and, despite great efforts to understand the underlying mechanisms that lead to cardiac and digestive manifestations in chronic patients, much remains to be clarified. The disease is found beyond Latin America, including Japan, the USA, France, Spain, and Australia, and is caused by the protozoan Trypanosoma cruzi. Dr. Carlos Chagas described Chagas disease in 1909 in Brazil, and hepatomegaly was among the clinical signs observed. Currently, hepatomegaly is cited in most papers published which either study acutely infected patients or experimental models, and we know that the parasite can infect multiple cell types in the liver, especially Kupffer cells and dendritic cells. Moreover, liver damage is more pronounced in cases of oral infection, which is mainly found in the Amazon region. However, the importance of liver involvement, including the hepatic immune response, in disease progression does not receive much attention. In this review, we present the very first paper published approaching the liver’s participation in the infection, as well as subsequent papers published in the last century, up to and including our recently published results. We propose that, after infection, activated peripheral T lymphocytes reach the liver and induce a shift to a pro-inflammatory ambient environment. Thus, there is an immunological integration and cooperation between peripheral and hepatic immunity, contributing to disease control.

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Human acute Chagas disease: changes in factor VII, activated protein C and hepatic enzymes from patients of oral outbreaks in Pará State (Brazilian Amazon)

Cited by 8 publications

References 23 publications

Prognosis of chronic Chagas heart disease and other pending clinical challenges

Prognosis of chronic Chagas heart disease and other pending clinical challenges

In the Acute Phase of Trypanosoma cruzi Infection, Liver Lymphoid and Myeloid Cells Display an Ambiguous Phenotype Combining Pro- and Anti-Inflammatory Markers

The Liver and the Hepatic Immune Response in Trypanosoma cruzi Infection, a Historical and Updated View

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