scholarly journals Genetic Structure and Expression of the Surface Glycoprotein GP82, the Main Adhesin ofTrypanosoma cruziMetacyclic Trypomastigotes

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Paulo Roberto Ceridorio Correa ◽  
Esteban Mauricio Cordero ◽  
Luciana Girotto Gentil ◽  
Ethel Bayer-Santos ◽  
José Franco da Silveira
Keyword(s):  
Host Cell ◽  
Cell Invasion ◽  
Secretory Pathway ◽  
Surface Protein ◽  
Surface Glycoprotein ◽  
Modular Organization ◽  
Transcriptional Level ◽  
Host Cell Invasion ◽  
Mrna Stabilization ◽  
Transgenic Parasites

T. cruziimproves the likelihood of invading or adapting to the host through its capacity to present a large repertoire of surface molecules. The metacyclic stage-specific surface glycoprotein GP82 has been implicated in host cell invasion. GP82 is encoded by multiple genes from the trans-sialidase superfamily. GP82 shows a modular organization, with some variation of N-terminal region flanking a conserved central core where the binding sites to the mammalian cell and gastric mucin are located. The function of GP82 as adhesin in host cell invasion process could expose the protein to an intense conservative and selective pressure. GP82 is a GPI-anchored surface protein, synthesized as a 70 kDa precursor devoid ofN-linked sugars. GPI-minus variants accumulate in the ER indicating that GPI anchor acts as a forward transport signal for progressing along the secretory pathway as suggested forT. cruzimucins. It has been demonstrated that the expression of GP82 is constitutive and may be regulated at post-transcriptional level, for instance, at translational level and/or mRNA stabilization. GP82 mRNAs are mobilized to polysomes and consequently translated, but only in metacyclic trypomastigotes. Analysis of transgenic parasites indicates that the mechanism regulating GP82 expression involves multiple elements in the 3′UTR.

scholarly journals Structural insights into an atypical secretory pathway kinase crucial for Toxoplasma gondii invasion

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Gaëlle Lentini ◽  
Rouaa Ben Chaabene ◽  
Oscar Vadas ◽  
Chandra Ramakrishnan ◽  
Budhaditya Mukherjee ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Host Cell ◽  
Cell Invasion ◽  
Plasma Membranes ◽  
Secretory Pathway ◽  
Host Cell Invasion ◽  
Host Cell Membrane ◽  
Apicomplexan Parasites ◽  
Cell Plasma ◽  
Structural Insights

AbstractActive host cell invasion by the obligate intracellular apicomplexan parasites relies on the formation of a moving junction, which connects parasite and host cell plasma membranes during entry. Invading Toxoplasma gondii tachyzoites secrete their rhoptry content and insert a complex of RON proteins on the cytoplasmic side of the host cell membrane providing an anchor to which the parasite tethers. Here we show that a rhoptry-resident kinase RON13 is a key virulence factor that plays a crucial role in host cell entry. Cryo-EM, kinase assays, phosphoproteomics and cellular analyses reveal that RON13 is a secretory pathway kinase of atypical structure that phosphorylates rhoptry proteins including the components of the RON complex. Ultimately, RON13 kinase activity controls host cell invasion by anchoring the moving junction at the parasite-host cell interface.

scholarly journals Reduced Adherence and Host Cell Invasion by Methicillin‐ResistantStaphylococcus aureusExpressing the Surface Protein Pls

2004 ◽  
Vol 189 (9) ◽  
pp. 1574-1584 ◽  
Author(s):  
Katri M. Juuti ◽  
Bhanu Sinha ◽  
Cornelia Werbick ◽  
Georg Peters ◽  
Pentti I. Kuusela
Keyword(s):  
Host Cell ◽  
Cell Invasion ◽  
Surface Protein ◽  
Host Cell Invasion ◽  
Reduced Adherence

scholarly journals A Genome-Wide siRNA Screen Implicates Spire1/2 in SipA-Driven Salmonella Typhimurium Host Cell Invasion

PLoS ONE ◽  
2016 ◽  
Vol 11 (9) ◽  
pp. e0161965 ◽  
Author(s):  
Daniel Andritschke ◽  
Sabrina Dilling ◽  
Mario Emmenlauer ◽  
Tobias Welz ◽  
Fabian Schmich ◽  
...  
Keyword(s):  
Salmonella Typhimurium ◽  
Host Cell ◽  
Cell Invasion ◽  
Host Cell Invasion ◽  
Sirna Screen ◽  
Genome Wide ◽  
A Genome

Characterisation of NcGRA7 and NcSAG4 proteins: Immunolocalisation and their role in the host cell invasion by Neospora caninum tachyzoites

2010 ◽  
Vol 55 (4) ◽  
Author(s):  
Adriana Aguado-Martínez ◽  
Gema Álvarez-García ◽  
Gereon Schares ◽  
Verónica Risco-Castillo ◽  
Aurora Fernández-García ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Host Cell ◽  
Cell Invasion ◽  
Neospora Caninum ◽  
Parasitophorous Vacuole ◽  
Membrane Surface ◽  
Chronic Phase ◽  
Host Cell Invasion ◽  
Invasion Mechanisms ◽  
The Matrix

AbstractNeospora caninum negatively impacts bovine reproductive performance around the world. Addressing this problem requires a greater understanding of the parasite’s molecular biology. In this study, monoclonal antibodies against recombinant proteins were successfully developed and employed to characterise two different proteins of N. caninum: the acute phase-associated NcGRA7 and the chronic phase-associated NcSAG4. Immunofluorescence with the anti-rNcGRA7 monoclonal antibody suggested that NcGRA7 trafficks from tachyzoite dense granules to the matrix of the parasitophorous vacuole and parasite’s surroundings. Furthermore, NcGRA7 is also expressed in the bradyzoite stage and localised on the matrix of bradyzoite-positive vacuoles. NcGRA7 appears to be partially involved in the tachyzoite-invasion mechanisms, as an anti-rNcGRA7 monoclonal antibody partially inhibited in vitro tachyzoite-invasion. A monoclonal antibody specific for NcSAG4 confirmed this protein’s bradyzoitespecific expression both by western blot and immunofluorescence. However, some bradyzoite-positive vacuoles only weakly expressed NcSAG4, if it was expressed at all. The specificity of the anti-rNcSAG4 monoclonal antibody was confirmed by the recognition of the NcSAG4 in the membrane surface of Nc-1SAG4c transgenic tachyzoites, which constitutively expresses NcSAG4. Blocking NcSAG4 of Nc-1SAG4c tachyzoites with the monoclonal antibody did not affect host cell invasion. However, its implication on the host cell adhesion or host immune evasion should not be discarded.

scholarly journals 1,3,4-Thiadiazoles Effectively Inhibit Proliferation of Toxoplasma gondii

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1053
Author(s):  
Lidia Węglińska ◽  
Adrian Bekier ◽  
Katarzyna Dzitko ◽  
Barbara Pacholczyk-Sienicka ◽  
Łukasz Albrecht ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Host Cell ◽  
Cell Invasion ◽  
Direct Action ◽  
Human Fibroblasts ◽  
Imidazole Ring ◽  
Host Cells ◽  
In Vitro Assays ◽  
Host Cell Invasion

Congenital and acquired toxoplasmosis caused by the food- and water-born parasite Toxoplasma gondii (T. gondii) is one of the most prevalent zoonotic infection of global importance. T. gondii is an obligate intracellular parasite with limited capacity for extracellular survival, thus a successful, efficient and robust host cell invasion process is crucial for its survival, proliferation and transmission. In this study, we screened a series of novel 1,3,4-thiadiazole-2-halophenylamines functionalized at the C5 position with the imidazole ring (1b–12b) for their effects on T. gondii host cell invasion and proliferation. To achieve this goal, these compounds were initially subjected to in vitro assays to assess their cytotoxicity on human fibroblasts and then antiparasitic efficacy. Results showed that all of them compare favorably to control drugs sulfadiazine and trimethoprim in terms of T. gondii growth inhibition (IC50) and selectivity toward the parasite, expressed as selectivity index (SI). Subsequently, the most potent of them with meta-fluoro 2b, meta-chloro 5b, meta-bromo 8b, meta-iodo 11b and para-iodo 12b substitution were tested for their efficacy in inhibition of tachyzoites invasion and subsequent proliferation by direct action on established intracellular infection. All the compounds significantly inhibited the parasite invasion and intracellular proliferation via direct action on both tachyzoites and parasitophorous vacuoles formation. The most effective was para-iodo derivative 12b that caused reduction in the percentage of infected host cells by 44% and number of tachyzoites per vacuole by 93% compared to non-treated host cells. Collectively, these studies indicate that 1,3,4-thiadiazoles 1b–12b, especially 12b with IC50 of 4.70 µg/mL and SI of 20.89, could be considered as early hit compounds for future design and synthesis of anti-Toxoplasma agents that effectively and selectively block the invasion and subsequent proliferation of T. gondii into host cells.

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