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• W2073669687 abstract "Chagas disease is a parasitic infection, and itsmain manifestations are the cardiac and digestiveforms. In the chronic cardiac form, on a signifi-cant number of cases, a severe cardiomyopathy isdeveloped. A therapeutic alternative in the Chagasdisease evolution of a patient with terminal chronicchagasic myocarditis could be the rehabilitationthrough a cardiac transplantation (Boullon et al.1988). These patients are submitted to immuno-suppressive therapy in order to prevent graft re-jection (Bocchi 1987, Stolf et al. 1987, Almeida etal. 1996).Over the last years, new aspects have surfacedthrough the association of Chagas disease with theacquired immunodeficiency syndrome (Aids) (DelCastillo et al. 1990, Gluckstein & Silva 1992, Oddoet al. 1992, Rocha et al. 1994, Ferreira et al. 1997).Chagas disease in immunocompromissed hosts isnot exclusively associated to Aids, but also to theaction of immunosuppressive drugs that are appliedin cancer and transplant chemotherapy (Bocchi1987, Jatene 1987, Stolf et al. 1987, Uip et al.1987).After an acute phase of Chagas disease in whicha “clinical cure” is obtained through chemotherapyor in assymptomatic cases, the parasite/host rela-tionship is disturbed only when a treatment withimmunosuppressive drugs is introduced. It has beendemonstrated that immunosuppressive drugs canmodulate both cell mediated immunity and anti-body production, thus affecting concomitant im-munity (or premunition). On the other hand, whensome immunosuppressive drugs are given beforeinfection they may promote an enhancement of cellmediated immunity and, paradoxaly, induce resis-tance against facultative intracellular parasites(Tripathy & Mackaness 1969, Goncalves da Costa& Lagrange 1981).In the past, cyclophosphamide (CY) was usedin the immunosuppressive therapy for the cardiactransplant. At this moment, the most used therapyis a treatment schedule formed by cyclosporin A(CsA), azatioprin and a corticoid (Ferraz &Figueiredo 1993).Experimental use of immunosuppressive drugsdemonstrated that CY injected after Trypanosomacruzi infection induces an enhancement of myo-carditis (Kumar et al. 1970).This was confirmedby Andrade et al. (1987) in dogs as well as in miceby Calabrese et al. (1987) and Silva and Rossi(1990).The action of this drug is dose and time depen-dent as observed in a experimental schedule usinghigh dose of CY before or after infection with T.cruzi Y strain. Mice treated by a single dose of200 mg/kg of CY two days before infection had afirst parasitaemic peak on day five which washigher than the control group. After that, the courseof the infection was similar to the infected non-treated control group. On the other hand, micetreated five days after infection with the same dosedisplayed a constant and higher ascendantparasitaemia. Animals treated with therapeuticdoses (3 mg/kg) show the same result as micetreated with high dose five days after infection.The analysis of blood cells, on animals treatedfive days after infection showed waves of leuko-cytes with a reduced number of cells on the 8thday after infection, the day of the parasitaemiapeak of the Y strain. This justifies a small numberof cells in inflammatory infiltrate on the heart onday 12 after infection. As CY is a cytotoxic drug,at this time the cells are suppressed. However thegroup treated two days before infection showed agreat inflammatory infiltrate on the heart accord-ing to the great number of leukocytes circulatingon blood because the toxic effect had already fin-ished. The results of therapeutic doses (3 mg/kg)showed a great number of circulating leukocytes.The specific analysis of these cells in the bloodshowed an enhancement of polymorphonuclear andmonocytes cells seven days after the injection ofthe drug on animals treated two days before infec-" @default.
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• W2073669687 date "1999-09-01" @default.
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• W2073669687 title "Immunosuppressive drugs as a tool to explore immunopathology in experimental Chagas disease" @default.
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• W2073669687 doi "https://doi.org/10.1590/s0074-02761999000700046" @default.
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