Immunopathology of cardiomyopathy in the experimental Chagas disease

Soares, Milena Botelho Pereira; Santos, Ricardo Ribeiro dos

doi:10.1590/s0074-02761999000700043

Cited by 30 publications

(20 citation statements)

References 28 publications

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“…Some authors propose that myocardial damage may be related to microvascular abnormalities leading to local ischemia and focal pathological changes (Rossi and Ramos 1996). Others have suggested that autoimmune reactions may be involved in the generation of tissue lesions (Soares and Ribeiro Dos Santos 1999), with tissue persistence of parasite antigens being involved in the disruption of self-tolerance regulatory mechanisms (Tarleton et al 1997). Whatever the precise mechanism, both processes can ultimately lead to the expression of in¯ammatory cytokines and adhesion molecules usually seen in the myocardium of mice and humans with this trypanosomal infection (Reis et al 1993;Zhang and Tarleton 1996;Tarleton et al 1997;Huang et al 1999).…”

Section: Discussionmentioning

confidence: 99%

Treatment with benznidazole and its immunomodulating effects on Trypanosoma cruzi -infected rats

Piaggio¹,

Roggero²,

Pitashny³

et al. 2001

Parasitology Research

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Because benznidazole (BZL) was found to downregulate nitric oxide (NO) and cytokine synthesis by murine macrophages, we analyzed the potential immunological repercussions of BZL treatment in Trypanosoma cruzi-infected rats. To evaluate whether the effects of BZL were also observed in the presence of an immunostimulating cytokine, four groups of acutely infected rats were subjected to one of the following 20-day therapeutic schedules: (1) a curative BZL oral regimen, (2) recombinant interferon (IFN-gamma) injections, (3) a suboptimal BZL regimen (25% of curative dose), (4) the latter plus IFN-gamma. All BZL doses markedly reduced NO-derived metabolites either in the circulation or in cultured macrophage supernatants. This was observed in rats simultaneously treated with IFN-gamma, which contrasted with the augmented NO production seen in animals given this cytokine alone. The untreated rats, and groups receiving monotherapy with IFN-gamma or 25% BZL, had increased circulating interleukin (IL)-1beta and IL-2 levels, which were reduced in those given BZL plus IFN-gamma. Although combined treatment failed to cause the virtually undetectable blood parasite levels induced by optimal BZL doses, chronic myocardial lesions were reduced to the same extent as in those receiving the curative schedule. The beneficial effects of BZL in this trypanosomiasis may also depend on some immunomodulating influences.

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Section: Discussionmentioning

confidence: 99%

Treatment with benznidazole and its immunomodulating effects on Trypanosoma cruzi -infected rats

Piaggio¹,

Roggero²,

Pitashny³

et al. 2001

Parasitology Research

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“…Although often they are not associated with amastigote nests or trypomastigotes, T. cruzi antigens may be present (Higuchi 1995, Reis et al 1997). CD4 + T cells, though less prominent in the chronic stage, are suggested to be associated with myocyte death and increased animal mortality (Soares et al 2001) and appear to represent an autoreactive phenotype that contributes to tissue destruction (Soares and Santos 1999). At this later stage, continued production of IFN-γ and IL-2 is believed to stimulate lytic antibody production by B cells (Brener and Gazzinelli 1997).…”

Section: Experimental Studiesmentioning

confidence: 99%

An overview of chagasic cardiomyopathy: pathogenic importance of oxidative stress

Zacks

Wen

Vyatkina

et al. 2005

An. Acad. Bras. Ciênc.

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There is growing evidence to suggest that chagasic myocardia are exposed to sustained oxidative stressinduced injuries that may contribute to disease progression. Pathogen invasion-and replication-mediated cellular injuries and immune-mediated cytotoxic reactions are the common source of reactive oxygen species (ROS) in infectious etiologies. However, our understanding of the source and role of oxidative stress in chagasic cardiomyopathy (CCM) remains incomplete. In this review, we discuss the evidence for increased oxidative stress in chagasic disease, with emphasis on mitochondrial abnormalities, electron transport chain dysfunction and its role in sustaining oxidative stress in myocardium. We discuss the literature reporting the consequences of sustained oxidative stress in CCM pathogenesis.Key words: chagasic cardiomyopathy, reactive oxygen species, inflammation, mitochondria, oxidant/antioxidant status, oxidative damage. PARASITE, VECTOR AND TRANSMISSIONTrypanosoma cruzi, a parasitic protozoan of the ancient branch of eukaryotes (Kingdom Eukaryota, Order Kinetoplastida), is the etiological agent of Chagas disease in humans (Miles 2003). Currently, the World Health Organization estimates that 11-18 million individuals are infected worldwide (WHO 2002). Transmission of T. cruzi occurs predominantly via insect vectors of the subfamily Triatoma, family Reduviidae, referred to as " kissing bugs". Residing in the peridomestic habitat of mud-thatch Correspondence to: Nisha Garg Ph.D. E-mail: nigarg@utmb.edu houses in rural areas (Mott et al. 1978), Triatoma infestans in South America, Rhodnius prolixus in Venezuela, Colombia and Central America (Schofi eld and Dias 1999), and Triatoma barberi in Mexico (Guzman 2001), are the most common species responsible for transmission. Improvements in housing conditions and vector control measures instituted by the Southern Cone Initiative in 1991 have contributed to a decline in transmission in endemic countries (Schofi eld and Dias 1999). However, concern remains that reinfestation of homes by secondary sylvatic vectors, e.g. Triatoma sordida, will compromise the long-term effi cacy of vector control measures in Brazil and other Southern American countries (Monteiro et al. 2001, WHO 2002. Blood transfusion and organ transplantation represent further routes of T. cruzi transmission. Although many countries in Latin America screen blood donations for T. cruzi, infection rates ranging from 0.1% to 24.4% are estimated to occur through transfusion (WHO 2002).In the U.S., vector-transmitted human infections have been reported in the southern States (Ochs et al. 1996, Herwaldt et al. 2000. Several studies have shown the presence of the insect vector as well as infection of domestic dogs and wild animals in the US (Meurs et al. 1998, Bradley et al. 2000, Beard et al. 2003, Yabsley and Noblet 2002. Further, due to signifi cant increases in immigration to the USA and Canada from endemic countries and perinatal transmission, it is estimated that ∼ 100, 000 people residing...

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“…The acute phase is characterized by parasites found throughout the body, replicating within macrophages and a variety of other host cells, especially cardiac muscle cells. It is histopathologically characterized by inflammatory infiltration and tissue necrosis (Soares & Ribeiro dos Santos 1999). Following an acute infection, the chronic phase is characterized by a variable clinical course ranging from absence of symptoms to severe cardiac and/or gastrointestinal involvement (Macedo et al 2002).…”

mentioning

confidence: 99%

Trypanosoma cruzi: parasite persistence in tissues in chronic chagasic Brazilian patients

Marcon

Albuquerque

Batista

et al. 2011

Mem. Inst. Oswaldo Cruz

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Immunopathology of cardiomyopathy in the experimental Chagas disease

Abstract: The mechanisms by which Trypanosoma cruzi causes cardiomyopathy and induces neuronal destruction

Cited by 30 publications

References 28 publications

Treatment with benznidazole and its immunomodulating effects on Trypanosoma cruzi -infected rats

Treatment with benznidazole and its immunomodulating effects on Trypanosoma cruzi -infected rats

An overview of chagasic cardiomyopathy: pathogenic importance of oxidative stress

Trypanosoma cruzi: parasite persistence in tissues in chronic chagasic Brazilian patients

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