Experimental Chagas' Disease: Electrophysiology and Cell Composition of the Neuromyopathic Inflammatory Lesions in Mice Infected with a Myotropic and a Pantropic Strain of Trypanosoma cruzi

Mirkin, Gerardo A.; Jones, Marta; Sanz, Olga; Rey, Roberto; Sica, R. E. P.; Cappa, Stella U.González

doi:10.1006/clin.1994.1171

Cited by 39 publications

(25 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This finding as well as the detection of parasites and parasite kDNA in the parasite-injected transplanted heart preceding the inflammatory process provides compelling evidence of a causal link between the presence of parasites in tissues and the inflammatory disease process. The proposed link between parasite load and disease severity in T. cruzi infection is also supported by a growing body of evidence connecting disease severity with the virulence of the infecting parasites (28,29), the persistence of parasites in the diseased tissues (30)(31)(32)(33), and the efficacy of anti-parasite chemotherapy (34)(35)(36).…”

Section: Discussionmentioning

confidence: 94%

“Autoimmune rejection” of neonatal heart transplants in experimental Chagas disease is a parasite-specific response to infected host tissue

Tarleton

Zhang

Downs

1997

Proc. Natl. Acad. Sci. U.S.A.

133

View full text Add to dashboard Cite

Infection with the protozoan parasite Trypanosoma cruzi often results in chronic heart-and gutassociated disease known as Chagas disease. In this study we show that contrary to previous reports, neonatal hearts transplanted into mice chronically infected with T. cruzi do not exhibit signs of autoimmune-type rejection or any significant inf lammatory response. In addition to an absence of inf lammation, these syngeneic heart transplants survive for more than 1 year and are absolutely free of parasites as determined by in situ PCR analysis. However, if well-established transplanted hearts in chronically infected mice are directly injected with live parasites, a rapid and dramatic inf lammatory response ensues that results in cessation of heart function. Likewise, transplanted hearts established in mice prior to systemic infection with T. cruzi or hearts transplanted into mice during the acute stage of T. cruzi infection become parasitized and develop inf lammatory foci. In these cases where the transplanted hearts become parasitized, the ensuing inf lammatory response is nearly identical to that observed in the native hearts of T. cruzi-infected mice in terms of cell types present and adhesion molecules and cytokines expressed. Importantly, this response is strikingly different from that observed in the allogeneic heart rejection. These results clearly document that parasitization of heart tissue is both necessary and sufficient for the induction of tissue damage in Chagas disease and strongly argue against a principal autoimmune etiology for this disease.

show abstract

Section: Discussionmentioning

confidence: 94%

“Autoimmune rejection” of neonatal heart transplants in experimental Chagas disease is a parasite-specific response to infected host tissue

Tarleton

Zhang

Downs

1997

Proc. Natl. Acad. Sci. U.S.A.

133

View full text Add to dashboard Cite

show abstract

“…Thus, it is relevant to understand the participation of NK cells in the maturation or elimination of the iDCs in the context of T. cruzi infection. Therefore, we used experimental murine infection with two parasite populations displaying significant biological differences: RA is a highly virulent (HV), fast-duplicating, pantropic strain belonging to the TcVI lineage isolated from an acutely infected child [20] whereas K98 is a slow-duplicating, myotropic strain with low virulence (LV) belonging to TcI isolated from a chronically infected adult [21,22,23,24]. Here, we show that iDCs subsets start to accumulate in the spleen very early upon infection with the HV strain but not with the LV strain.…”

Section: Introductionmentioning

confidence: 99%

Impairment in Natural Killer Cells Editing of Immature Dendritic Cells by Infection with a Virulent <b><i>Trypanosoma cruzi</i></b> Population

Batalla

Martínez

Poncini³

et al. 2013

J Innate Immun

View full text Add to dashboard Cite

Early interactions between natural killer (NK) and dendritic cells (DC) shape the immune response at the frontier of innate and adaptive immunity. Activated NK cells participate in maturation or deletion of DCs that remain immature. We previously demonstrated that infection with a high virulence (HV) population of the protozoan parasite Trypanosoma cruzi downmodulates DC maturation and T-cell activation capacity. Here, we evaluated the role of NK cells in regulating the maturation level of DCs. Shortly after infection with HV T. cruzi, DCs in poor maturation status begin to accumulate in mouse spleen. Although infection induces NK cell cytotoxicity and cytokine production, NK cells from mice infected with HV T. cruzi exhibit reduced ability to lyse and fail to induce maturation of bone marrow-derived immature DCs (iDCs). NK-mediated lysis of iDCs is restored by in vitro blockade of the IL-10 receptor during NK-DC interaction or when NK cells are obtained from T. cruzi-infected IL-10 knockout mice. These results suggest that infection with a virulent T. cruzi strain alters NK cell-mediated regulation of the adaptive immune response induced by DCs. This regulatory circuit where IL-10 appears to participate might lead to parasite persistence but can also limit the induction of a vigorous tissue-damaging T-cell response.

show abstract

“…Durante la fase aguda, el parásito ingresa al individuo y puede producir sintomatología en el paciente o no, lo que depende de factores como la cepa del parásito (111,112) y las características del huésped, que son las que modulan la reacción inicial (79). Por ejemplo, dependiendo de la cepa del parásito puede haber una mayor o menor lesión contra el sistema nervioso central, el músculo esquelético o los nervios periféricos, la que es mediada especialmente por los linfocitos T del tipo CD4 (113).…”

Section: Fisiopatologíaunclassified

Neurotripanosomiasis americana: aspectos clínicos de un problema básico.

León-Sarmiento¹,

Prada²,

Bayona-Prieto³

et al. 2003

biomedica

View full text Add to dashboard Cite

Trypanosoma cruzi es el agente causal de la enfermedad de Chagas, patología que afecta principalmente estructuras cardiacas e intestinales. Sin embargo, las complicaciones neurológicas no han sido adecuadamente identificadas y estudiadas en Colombia, a pesar de existir allí áreas geográficas que presentan prevalencias de infección iguales o mayores de las informadas en otras latitudes, en donde se le ha dado una mayor atención a este tipo de complicaciones, desde hace ya varios años. Realizamos un metanálisis cualitativo sobre el tema, en la base de datos PubMed, en el motor de búsqueda Altavista y en las revistas colombianas indexadas por Colciencias, así como en tres libros que trataban el tópico de manera específica. Usamos las palabras claves: Trypanosoma, Chagas' disease, nervous system, spinal cord, central nervous system, peripheral nervous system, neuromuscular junction, autonomic nervous system, muscle, muscle disorders, neuromuscular disease, neuromuscular disorders, synapticopathies y dysautonomia. Como criterio de inclusión se debía haber realizado e informado la prueba de ELISA, inmunofluorescencia indirecta, presencia de parasitemia o presencia de parásitos en los tejidos, dependiendo de si se trataba de un estudio clínico-serológico o histopatólogico. No tuvimos en cuenta como criterio de inclusión la realización de la prueba de reacción en cadena de la polimerasa, dado que sólo hasta épocas recientes se introdujo esta técnica en el estudio de esta patología en Colombia. Encontramos 116 manuscritos con los términos antes descritos; éstos incluían artículos originales, revisiones, informe de casos, editoriales y comunicaciones breves, así como conferencias y capítulos de libros que cumplieron con los requisitos planteados. En ellos se apreció claramente cómo la enfermedad de Chagas afecta todos los niveles del sistema nervioso central, periférico y autonómico, siendo este último sistema el que se ha estudiado con mayor profundidad en nuestro país. Consideramos que el compromiso neurosistémico producido por T. cruzi debe ser evaluado de una manera más profunda a partir de la fecha, dado que muchos de los pacientes pueden estar siendo diagnosticados, tratados y seguidos como portadores de enfermedades 'idiopáticas'. Dichas patologías pueden llegar a convertirse en una seria amenaza para la salud de muchos colombianos si no se toman las medidas de prevención y control adecuadas. Por tanto, es necesario que actuemos en consecuencia, de acuerdo con el espectro de anormalidades neurológicas que se presentan en estos pacientes, como lo demostramos en el presente trabajo.

show abstract

Experimental Chagas' Disease: Electrophysiology and Cell Composition of the Neuromyopathic Inflammatory Lesions in Mice Infected with a Myotropic and a Pantropic Strain of Trypanosoma cruzi

Cited by 39 publications

References 0 publications

“Autoimmune rejection” of neonatal heart transplants in experimental Chagas disease is a parasite-specific response to infected host tissue

“Autoimmune rejection” of neonatal heart transplants in experimental Chagas disease is a parasite-specific response to infected host tissue

Impairment in Natural Killer Cells Editing of Immature Dendritic Cells by Infection with a Virulent <b><i>Trypanosoma cruzi</i></b> Population

Neurotripanosomiasis americana: aspectos clínicos de un problema básico.

Contact Info

Product

Resources

About