Cytokine Production in Hearts of <i>Trypanosoma cruzi</i>‐Infected CBA Mice: Do Cytokine Patterns in Chronic Stage Reflect the Establishment of Myocardial Pathology?

Sunnemark, Dan; Ulfgren, Ann‐Kristin; Örn, Anders; Harris, Robert A.

doi:10.1046/j.1365-3083.1996.d01-328.x

Cited by 24 publications

(23 citation statements)

References 50 publications

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“…In our study of chronic inflammation in the heart [15] we were not able to detect interferon-g (IFN-g) or intracellular parasites, which concords with the lack of iNOS expression and parasites in the present study. Neuraminidase, a parasite enzyme, has been reported to promote adhesion of platelets and polymorphonuclear cells to the endothelium in vitro [25].…”

Section: Vasculitis In Murine T Cruzi Infection 481supporting

confidence: 76%

“…Experimental T. cruzi infection results in severe pathological changes in the hearts of infected CBA mice, characterized by extensive infiltration of T cells and macrophages with associated production of cytokines [15]. Our current study focused on investigation of potential inflammatory events occurring both in proximity to the heart (aortal sinus) and distal to the heart (in the descending aorta) in T. cruzi-infected mice.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to vascular damage, infection with T. cruzi induces proinflammatory cytokine production in the myocardium itself [15,19], which may further exacerbate the pathology and adversely affect myocardial function.…”

Section: Discussionmentioning

confidence: 99%

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Cellular and Cytokine Characterization of Vascular Inflammation in CBA/J Mice Chronically Infected with Trypanosoma cruzi

et al. 1998

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Continuing our characterization of the immunopathological events occurring during experimental murine Chagas' disease, an immunohistological examination was conducted of the aortas of chronically infected CBA/J mice. Compared with non‐infected mice of identical age, Trypanosoma cruzi‐infected mice exhibited a marked vasculitis, with significant infiltration of inflammatory cells into the adventitial layer, including CD4+, CD8+ T cells and macrophages. Production of interleukin‐6 (IL‐6) and tumour necrosis factor‐α (TNF‐α) was evident in the inflammatory infiltrate in the endothelial and smooth muscle layers. Vasculitis was most apparent in proximity to the heart, but extended along the aorta. Such an inflammation could lead to an alteration of the endothelium, altering the protective properties of this layer and further contributing to the focal pathology characteristic of this stage of infection.

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Section: Vasculitis In Murine T Cruzi Infection 481supporting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

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Cellular and Cytokine Characterization of Vascular Inflammation in CBA/J Mice Chronically Infected with Trypanosoma cruzi

et al. 1998

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“…Previous studies have argued that type 2 cytokine responses may increase the severity of disease in acute and chronic T. cruzi infection (40,(42)(43)(44), or alternately may reduce the severity of disease by modulating a potentially overactive type 1 cytokine response (10,38,45). The most dramatic example of exacerbation of inflammatory disease resulting from manipulation of cytokine production patterns in T. cruzi infection comes from studies with IL-10 Ϫ/Ϫ mice infected with T. cruzi.…”

Section: Discussionmentioning

confidence: 99%

Increased Susceptibility of Stat4-Deficient and Enhanced Resistance in Stat6-Deficient Mice to Infection withTrypanosoma cruzi

Tarleton

Grusby

Zhang

2000

The Journal of Immunology

103

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Although Th1-type responses tend to be associated with resistance to Trypanosoma cruzi infection, mixed Th1 and Th2 cytokine responses are generally observed in both resistant and susceptible mice. To help clarify the role of type 1 and type 2 cytokine responses in immunity to T. cruzi, mice with induced deficiencies in the Stat4 or Stat6 genes were infected with T. cruzi. As expected, Stat4−/− mice deficient in type 1 cytokine responses were highly susceptible to infection, exhibiting increased parasitemia levels relative to wild-type mice and 100% mortality. In contrast, parasitemia levels and survival in Stat6-deficient mice were not different from wild type. The type 1 and type 2 cytokine bias of Stat6- and Stat4-deficient mice, respectively, was confirmed by in situ immunocytochemical analysis of cytokine-producing cells in the tissues of infected mice and by subclass analysis of anti-T. cruzi serum Abs. Notably, both Stat4- and Stat6-deficient mice produced substantial amounts of anti-T. cruzi Abs. Tissues from chronically infected Stat6-deficient mice had little to no evidence of inflammation in the heart and skeletal muscle in contrast to wild-type mice, which exhibited substantial inflammation. In situ PCR analysis of these tissues provided evidence of the persistence of T. cruzi in wild-type mice, but no evidence of parasite persistence in Stat6-deficient mice. These data suggest that type 1 T cells are required for the development of immune control to T. cruzi, but that type 2 T cells contribute to parasite persistence and increased severity of disease.

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“…5,6 T. cruzi is the causative agent of Chagas disease, a major health problem in South and Central America where it is most commonly associated with progressive cardiomyopathy. 4 The aim of this study was to examine the skeletal muscle involvement in an experimental model of Chagas disease established earlier in our laboratory 17 and to compare the pattern of inflammation with human idiopathic inflammatory myopathies.…”

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confidence: 99%

CBA/J mice infected with Trypanosoma cruzi: An experimental model for inflammatory myopathies

et al. 2003

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Idiopathic inflammatory myopathies are inflammatory disorders of unknown origin, characterized by muscle weakness. The aim of our study was to establish and characterize an animal model for chronic inflammatory myopathy which would permit investigations of the role of T-cells in chronic myositis as well as of the mechanisms for muscle weakness in chronic inflammatory muscle disorders. CBA/J mice were infected with the protozoan parasite Trypanosoma cruzi. Immunohistochemistry was used to characterize the distribution and composition of inflammatory infiltrates, and demonstrated a chronic focal inflammation comprised mainly of T-cells and macrophages in infected mice. The inflammatory infiltrates were predominantly found in the endomysium and, to a lesser extent, in perivascular areas. CD8(+) T-cells were found to have invaded nonnecrotic muscle fibers. Degenerating muscle fibers were also found, as well as an increased number of central muscle nuclei. The murine model described in this article may be useful in studying certain aspects of idiopathic inflammatory myopathies such as the role of T-cells in chronic muscle inflammation and chronic myocytotoxicity.

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Cytokine Production in Hearts of Trypanosoma cruzi‐Infected CBA Mice: Do Cytokine Patterns in Chronic Stage Reflect the Establishment of Myocardial Pathology?

Cited by 24 publications

References 50 publications

Cellular and Cytokine Characterization of Vascular Inflammation in CBA/J Mice Chronically Infected with Trypanosoma cruzi

Cellular and Cytokine Characterization of Vascular Inflammation in CBA/J Mice Chronically Infected with Trypanosoma cruzi

Increased Susceptibility of Stat4-Deficient and Enhanced Resistance in Stat6-Deficient Mice to Infection withTrypanosoma cruzi

CBA/J mice infected with Trypanosoma cruzi: An experimental model for inflammatory myopathies

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