Regulation of lymphokine production in experimental and human chagas' disease

Tarleton, Rick L.

doi:10.1590/s0074-02761988000500009

Cited by 4 publications

(3 citation statements)

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“…Both humoral and cellular immunities are suppressed in experimental infections, and altered interleukin 2 (IL-2) concentrations are associated with this immunosuppressed state (257,262,263). Furthermore, it has been suggested that IL-2 may participate in disease-related autoimmune phenomena in mice (262).…”

Section: Pathogenesis Of the Acute Infectionmentioning

confidence: 99%

Chagas' disease

et al. 1992

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Chagas' disease, caused by Trypanosoma cruzi, is an important cause of morbidity in many countries in Latin America. The important modes of transmission are by the bite of the reduviid bug and blood transfusion. The organism exists in three morphological forms: trypomastigotes, amastigotes, and epimastigotes. The mechanism of transformation and differentiation is currently being explored, and signal transduction pathways of the parasites may be involved in this process. Parasite adherence to and invasion of host cells is a complex process involving complement, phospholipase, penetrin, neuraminidase, and hemolysin. Two clinical forms of the disease are recognized, acute and chronic. During the acute stage pathological damage is related to the presence of the parasite, whereas in the chronic stage few parasites are found. In recent years the roles of tumor necrosis factor, gamma interferon, and the interleukins in the pathogenesis of this infection have been reported. The common manifestations of chronic cardiomyopathy are arrhythmias and thromboembolic events. Autoimmune, neurogenic, and microvascular factors may be important in the pathogenesis of the cardiomyopathy. The gastrointestinal tract is another important target, and "mega syndromes" are common manifestations. The diagnosis and treatment of this infection are active areas of investigation. New serological and molecular biological techniques have improved the diagnosis of chronic infection. Exacerbations of T. cruzi infection have been reported for patients receiving immuno-suppressive therapy and for those with AIDS.

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Section: Pathogenesis Of the Acute Infectionmentioning

confidence: 99%

Chagas' disease

et al. 1992

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“…Cachexia is a common manifestation of inflammation, and is presumed to result from increased synthesis and release of cytokines, mainly TNF-a, IL-1, IL-6 and IFN-y, both in cancer (Langstein & Norton 1991, Billiau & Matthys 1992 and in infection (Tracey 1992). The infection of mice by Trypanosoma cruzi, the causative agent of Chagas' disease, is known to seriously disturb the cytokine network (Tarleton & Nabors 1991). Indeed, the production of IFN-y (Torrico et al 1991;McCabe, Meagher & Mullins 1991, Vandekerckhove et al 1994 and IL-6 (Truyens et al 1994) is enhanced in acutely infected animals, which are also primed to produce high levels of TNF-(r in response to exogenous endotoxin (Tarleton 1988, Starobinas et al 1991.…”

Section: Introductionmentioning

confidence: 99%

The cachexia associated with Trypanosoma cruzi acute infection in mice is attenuated by anti‐TNF‐a, but not by anti‐IL‐6 or anti‐IFN‐7 antibodies

Truyens¹,

Torrico

Angelo-Barrios

et al. 1995

Parasite Immunology

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BALB/c male mice acutely infected with Trypanosoma cruzi underwent a severe weight loss (around 20%, from day 18 to 31 post-infection), when compared to age-matched uninfected animals. Though mice regained weight later, when blood parasites were hardly detectable, wasting extended over the chronic phase of infection. The onset and the magnitude of weight loss were related to the mouse susceptibility to infection, since they were respectively earlier and higher in male mice which will die than in surviving ones, in males than in females, and in BALB/c than in B6D2 [(C57B1/6 x DBA/2)F1], a mouse strain more resistant to infection. Fat weight of infected mice (male BALB/c) was reduced by 60 to 80%, whereas lean mass was unaffected and water content rose by 6 to 10% in acute and chronic infection. Haematocrit was also decreased by 15-16% in acute infection. Animals failed to compensate their energetic loss since their food intake remained similar to that of uninfected animals. Injections of neutralizing anti-TNF-alpha monoclonal antibody into infected male mice, during the first two weeks but not later in infection, significantly attenuated the weight loss. Early administration of anti-IL-6 or anti-IFN-gamma MoAbs did not improve the mouse wasting. Taken together, these data show that TNF is a key agent of cachexia occurring in the acute T. cruzi infection in mice.

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“…In recent years, the role of cytokines in the pathogenesis of T. cruzi infections has been the subject of intense investigation. Both humoral and cellular immunities are suppressed in experimental infections, and altered interleukin 2 (IL-2) concentrations are associated with this immunosuppressed state (257,262,263). Furthermore, it has been suggested that IL-2 may participate in disease-related autoimmune phenomena in mice (262).…”

Section: Immune Mechanismsmentioning

confidence: 99%