Invasion of MDCK epithelial cells with altered expression of Rho GTPases by Trypanosoma cruzi amastigotes and metacyclic trypomastigotes of strains from the two major phylogenetic lineages

Fernandes, Adriana Barrinha; Mortara, Renato Arruda

doi:10.1016/j.micinf.2004.01.009

Cited by 43 publications

(45 citation statements)

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“…The results given here also differ from those of other authors who studied several strains, and these results observed a relationship between infectivity and genetic group (Mangia et al 2001;Fernandes and Mortara 2004;Risso et al 2004). This difference may be related to the fact that some of these authors carried out in vitro experiments using strains kept in the laboratory for a long time or to the fact that the strains used in this study showed different biological behavior because they were isolated from an endemic area in which strains from the sylvatic environment were considered a special case (Soccol et al 2002).…”

Section: Discussioncontrasting

confidence: 99%

Infectivity for mice of Trypanosoma cruzi I and II strains isolated from different hosts

et al. 2006

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In this paper, the infectivity for mice of Trypanosoma cruzi I and II strains isolated from sylvatic animals, triatomines, and humans is determined using fresh blood examination, hemoculture, culture of macerated organs, and polymerase chain reaction (PCR). Six strains were considered to have low infectivity (9.1-18.2%), five medium (27.3-45.4%), and one high (100.0%). Infectivity of T. cruzi strains isolated from sylvatic animals was significantly higher than that of strains isolated from humans and triatomines (p=0.0141). No significant difference was observed between the infectivity of T. cruzi I and II strains. The parasite was detected by fresh blood examination in one strain, by hemoculture and culture of macerated organs in four strains, and by PCR in all strains. We conclude that the infectivity is related to the host from which the strains were isolated, but the infectivity is not related to the genetic group of the parasite. We also conclude that the majority of the strains studied have low and medium infectivity for mice, and that PCR is an important tool to detect T. cruzi in strains with this biological characteristic.

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Section: Discussioncontrasting

confidence: 99%

Infectivity for mice of Trypanosoma cruzi I and II strains isolated from different hosts

et al. 2006

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“…3). Among the other genes on this pathway, other researchers previously identified the involvement of some in the T. cruzi-infection (6,31). It will be of interest to investigate the behavior of the remaining genes in order to understand the mechanism of intracellular growth and persistence of T. cruzi and to find the therapeutic target of this infectious disease.…”

Section: Cellular Pathway Analysismentioning

confidence: 99%

“…T. cruzi epimastigotes (Tulahuen strain) were maintained in same medium at 27 C, and then propagated at 37 C for 1 day. 1.0-2.0ϫ10 6 parasites were added to nearly confluent monolayers of NIH3T3 in culture dishes (diameter, 10 cm) and further incubated at 37 C under 5% CO 2 for 8 days. To ensure the infection, proliferated amastigotes were observed under a microscope.…”

Section: Cell Culture and Trypanosoma Cruzi Infectionmentioning

confidence: 99%

Microarray Analysis of Host Gene‐Expression during Intracellular Nests Formation of Trypanosoma cruzi Amastigotes

Imai¹,

Mimori

Kikuchi³

et al. 2005

Microbiology and Immunology

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The intracellular pathogens utilize numerous cellular components of host cells to advance the infection as well as to enter the host cell. Analyzing the host cellular response enables us to get a better understanding of the pathogenesis, and subsequently indicate possible therapeutic targets. We therefore analyzed gene‐expression profile of NIH3T3 fibroblast cells infected by Trypanosoma, a representative intracellular pathogen similar to Leishmania, using custom‐designed cDNA microarray consisting of 1,701 mKIAA cDNAs. Focusing on intracellular nest formation of Trypanosoma cruzi amastigotes, we profiled the host gene‐expression at 8 days post‐infection and found several degrees of change in 16 mKIAA genes. Among these genes, 10 were up‐regulated and 6 were down‐regulated. Assuming that these genes had important roles in the infection's progression, we performed semi‐quantitative RT‐PCR analysis and confirmed the gene expression change of 4 genes. Furthermore, 5 genes were mapped on cadherin signaling pathway using pathway analysis software. These results indicate significance of the host cellular pathway in the proliferative stage of Trypanosoma cruzi amastigotes.

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“…The efficiency in entering non-phagocytic mammalian cells may vary widely between T. cruzi strains and strains belonging to different phylogenetic lineages, and it has been well established that metacyclic trypomastigotes from CL strain (T. cruzi II) are highly invasive whereas parasites from the G strain (belonging to T. cruzi I) are poorly infective (Neira et al 2002). However, EA of highly infective strains such as Y and CL are poorly infective when compared to type I parasites, particularly from the G strain, showing the opposite behavior of the corresponding metacyclic trypomastigote forms (Mortara et al 1999;Fernandes and Mortara 2004). For metacyclic trypomastigotes, the developmental forms that initiate infection in mammalian hosts, the variability between these strains has been associated to the differential expression of surface glycoproteins that bind to target cells in a receptormediated manner and exhibit differential Ca 2+ signaling activities (Ruiz et al 1998;Yoshida et al 2000).…”

Section: Introductionmentioning

confidence: 99%

Cell invasion by Trypanosoma cruzi amastigotes of distinct infectivities: studies on signaling pathways

et al. 2006

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Trypanosoma cruzi metacyclic trypomastigotes of the major phylogenetic lineages use specific signaling pathways to invade host cells. Using a panel of drugs, we studied if the differences in the ability of extracellular amastigotes (EA) from G (T. cruzi I) and CL (T. cruzi II) strains to invade host cells could be associated to activation of specific signaling routes. Sonicated extracts from G or CL strain EA induced transient raises in HeLa cell intracellular Ca(2+) levels in a dose-dependent manner. Treatment of EA with drugs that affect Ca(2+) release from inositol-1,4,5-triphosphate-sensitive stores did not significantly affect the infectivity of either strain, whereas EA of both strains treated with ionomycin plus NH(4)Cl or nigericin that release Ca(2+) from acidocalcisomes had their infectivity reduced. Treatment of parasites with adenylate cyclase activator forskolin increased the infectivity of both strains towards HeLa cells. These data, taken together, suggest that, for host cell invasion, G and CL strain EA engage signaling pathways that lead to an increase of cyclic adenosine monophosphate and Ca(2+) mobilization from acidocalcisomes. Moreover, treatment of EA with genistein reduced by approximately 45% the invasion of HeLa cells by G but not by CL strain, implicating a protein tyrosine kinase in the process. In line with this, HeLa cell extracts contained a protein tyrosine kinase activity that mediated the phosphorylation of 87- and 175-kDa polypeptides of EA from G but not from CL strain. Regarding the target cell response, the activation of host PI3 kinase appears to be required for invasion by either strain as treatment of HeLa cells with wortmannin reduced EA infectivity. These data overall reinforce the concept that cell invasion by T. cruzi EA markedly differs from the process involving metacyclic trypomastigotes.

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Invasion of MDCK epithelial cells with altered expression of Rho GTPases by Trypanosoma cruzi amastigotes and metacyclic trypomastigotes of strains from the two major phylogenetic lineages

Cited by 43 publications

References 50 publications

Infectivity for mice of Trypanosoma cruzi I and II strains isolated from different hosts

Infectivity for mice of Trypanosoma cruzi I and II strains isolated from different hosts

Microarray Analysis of Host Gene‐Expression during Intracellular Nests Formation of Trypanosoma cruzi Amastigotes

Cell invasion by Trypanosoma cruzi amastigotes of distinct infectivities: studies on signaling pathways

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