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Review on Trypanosoma cruzi: Host Cell Interaction.
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Review on Trypanosoma cruzi: Host Cell Interaction.
Int J Cell Biol. 2010;2010:
Authors: de Souza W, de Carvalho TM, Barrias ES
Trypanosoma cruzi, the causative agent of Chagas' disease, which affects a large number of individuals in Central and South America, is transmitted to vertebrate hosts by blood-sucking insects. This protozoan is an obligate intracellular parasite. The infective forms of the parasite are metacyclic and bloodstream trypomastigote and amastigote. Metacyclic trypomastigotes are released with the feces of the insect while amastigotes and bloodstream trypomastigotes are released from the infected host cells of the vertebrate host after a complex intracellular life cycle. The recognition between parasite and mammalian host cell involves numerous molecules present in both cell types. Here, we present a brief review of the interaction between Trypanosoma cruzi and its host cells, mainly emphasizing the mechanisms and molecules that participate in the T. cruzi invasion process of the mammalian cells.
PMID: 20811486 [PubMed - in process]
Infectivity, Pathogenicity, and Virulence of Trypanosoma cruzi Isolates from Sylvatic Animals and Vectors, and Domestic Dogs from the United States in ICR Strain Mice and SD Strain Rats.
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Infectivity, Pathogenicity, and Virulence of Trypanosoma cruzi Isolates from Sylvatic Animals and Vectors, and Domestic Dogs from the United States in ICR Strain Mice and SD Strain Rats.
Am J Trop Med Hyg. 2010 Sep;83(3):519-22
Authors: Roellig DM, Yabsley MJ
Trypanosoma cruzi, the causative agent of Chagas disease, is widespread in the southern United States. In addition to detection in numerous wildlife host species, cases have been diagnosed in domestic dogs and humans. In the current investigation, groups of laboratory mice [Crl:CD1 (ICR)] were inoculated with one of 18 United States T. cruzi isolates obtained from a wide host range to elucidate their infectivity, pathogenicity, and virulence. In addition, laboratory rats (SD strain) were inoculated with four isolates. Mice and rats were susceptible to infection with all strains, but no morbidity or mortality was noted, which indicates that these T. cruzi isolates from the United States had low virulence for laboratory mice and rats.
PMID: 20810814 [PubMed - in process]
T-bet-independent effects of IL-12 family cytokines on regulation of Th17 responses to experimental T. cruzi infection.
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T-bet-independent effects of IL-12 family cytokines on regulation of Th17 responses to experimental T. cruzi infection.
J Leukoc Biol. 2010 Aug 31;
Authors: Cobb D, Hambright D, Smeltz RB
Tbx21 (i.e., T-bet) is an IFN-gamma-inducible transcription factor that promotes Th1 differentiation. Previously, we reported that Tbx21(-/-) mice develop a robust Th17 response to the parasite Trypanosoma cruzi, including CD4(+) T cell subsets producing IL-17 and IFN-gamma. Because of the known inhibitory effects of IFN-gamma on Th17 cells, the purpose of this study was to determine the contribution of IFN-gamma to regulation of Th17 differentiation during the course of T. cruzi infection. We observed that infection of IFN-gamma(-/-) or Stat-1(-/-) mice generated increased numbers of IL-17-producing cells. In sharp contrast to infected Stat-1(-/-) or Tbx21(-/-) mice, however, IFN-gamma(-/-) mice developed a lower overall Th17 response, suggesting that IFN-gamma was not required for T-bet-dependent activity, including T-bet-dependent expression of CXCR3. To determine if IFN-gamma could influence Th17 responses indirectly by acting on APCs, we neutralized IFN-gamma in cultures containing APC and T. cruzi antigens. Although anti-IFN-gamma increased IL-17 production modestly, anti-IFN-gamma and anti-IL-12 led to a significant enhancement of T. cruzi-specific IL-17 (P<0.01). In contrast to the inhibitory effects of IL-12, IL-23 was able to stimulate Tbx21(-/-) T cells and cause a striking increase in T. cruzi-specific IL-17. These data show that the IL-12 family of cytokines can influence Th17 responses in a T-bet-independent manner and that the effects of IFN-gamma are not necessarily related to its ability to induce T-bet expression in T cells.
PMID: 20807701 [PubMed - as supplied by publisher]
