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Abstract
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.
Highlights
Chagas disease was described in the interior of Brazil, but the triatomine vector species that transmit the disease are geographically distributed throughout Latin America and today include the southern United States
Hepatic Natural killer T (NKT) cells seem to be important in the process of multiple cell type activation, as CD1d-deficient mice showed a significant decrease in natural killer (NK), macrophage, neutrophil, and conventional B and T lymphocyte function in the liver after in vivo viral infection [94]
We evaluated if activated intrahepatic lymphocytes (IHL) play a systemic role in vivo after T. cruzi infection
Summary
Three different forms are found in the parasite’s life cycle, and all of them were described by Dr Chagas He observed epimastigote forms in the insects’ intestines, trypomastigote forms in the blood of patients and others hosts, and (intracellular) amastigote forms in vertebrate lungs. Many other scientists played an important role in describing various aspects of the disease and its pathogenesis In his first published paper in 1909, Dr Chagas himself acknowledged Dr Oswaldo Cruz for his invaluable contribution and mentoring. Dr Chagas became the first physician and scientist to describe an infectious disease in its entirety He introduced all the elements involved to the scientific and medical community: the causal agent (Trypanosoma cruzi); the vector (Triatoma infestans); wild and domiciled reservoirs (vertebrate animals); the clinical signs and symptoms; the diagnosis; the prognosis; the epidemiology; and the ecology with all the dynamics of the disease transmission. Identifying the recent chronic phase is remarkable; once clinical symptoms are entirely different from the acute phase, only about 30% of infected individuals will develop cardiac symptoms, usually decades after the acute phase, and blood parasitemia is subpatent
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