Article
Reduced secretion and expression of gelatinase profile in Toxoplasma gondii-infected human monocytic cells.
Laboratoire de Biochimie et Biologie Moléculaire, CNRS UMR 6198, IFR 53, UFR Médecine, Université de Reims Champagne-Ardenne, 51 rue Cognacq-Jay, 51095 Reims cedex, France.
Biochemical and Biophysical Research Communications (impact factor:
2.48).
08/2007;
359(2):298-303.
DOI:10.1016/j.bbrc.2007.05.089
pp.298-303
Source: PubMed
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Citations (0)
- Cited In (2)
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Article: Phospholipase C gamma and ERK1/2 Mitogen Activated Kinase Pathways are differentially modulated by Trypanosoma cruzi during tissue invasion in human placenta.
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ABSTRACT: Chagas' disease is caused by the haemophlagelated protozoan Trypanosoma cruzi (T. cruzi). During congenital transmission the parasite breaks down the placental barrier, however studies about the physiopathology of this process are scarce. Different signal transduction pathways are involved during cell invasion of the parasite. However, the possible role of those processes during tissue infection has not been studied. In the present study we analyzed the modulation of two signal transduction pathways, PLC-γ and ERK1/2 MAPK, during ex vivo infection of human placental chorionic villi explants. Chorionic villi from healthy woman placentas were incubated in the presence or absence of 105 or 106 T. cruzi trypomastigotes (DM28c strain) with or without specific inhibitors for each pathway. Effective infection was tested determining parasite DNA by PCR. The activation of PLC-γ and ERK1/2 MAPK signaling pathways was determined by western blotting and immunofluorescence. The low concentration of T. cruzi trypomastigotes activates both signaling pathways; however, the high concentration of parasite induces a modest activation of the PLC-γ pathway and impairs the ERK1/2 MAPK pathway activation. Interestingly, inhibition of any of those signaling pathways did not prevent parasite infection, as it was previously shown in cell cultures. We conclude that both signal transduction pathways are modulated during ex vivo T. cruzi infection of human placental chorionic villi explants.Experimental Parasitology 10/2012; · 2.12 Impact Factor -
Article: Moderate Champagne consumption promotes an acute improvement in acute endothelial-independent vascular function in healthy human volunteers.
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ABSTRACT: Epidemiological studies have suggested an inverse correlation between red wine consumption and the incidence of CVD. However, Champagne wine has not been fully investigated for its cardioprotective potential. In order to assess whether acute and moderate Champagne wine consumption is capable of modulating vascular function, we performed a randomised, placebo-controlled, cross-over intervention trial. We show that consumption of Champagne wine, but not a control matched for alcohol, carbohydrate and fruit-derived acid content, induced an acute change in endothelium-independent vasodilatation at 4 and 8 h post-consumption. Although both Champagne wine and the control also induced an increase in endothelium-dependent vascular reactivity at 4 h, there was no significant difference between the vascular effects induced by Champagne or the control at any time point. These effects were accompanied by an acute decrease in the concentration of matrix metalloproteinase (MMP-9), a significant decrease in plasma levels of oxidising species and an increase in urinary excretion of a number of phenolic metabolites. In particular, the mean total excretion of hippuric acid, protocatechuic acid and isoferulic acid were all significantly greater following the Champagne wine intervention compared with the control intervention. Our data suggest that a daily moderate consumption of Champagne wine may improve vascular performance via the delivery of phenolic constituents capable of improving NO bioavailability and reducing matrix metalloproteinase activity.The British journal of nutrition 11/2009; 103(8):1168-78. · 3.45 Impact Factor
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Keywords
48h post invasion
activation
apicomplexan Toxoplasma gondii
blood-brain barrier
decrease
infect humans
inhibition
matrix metalloproteinases
molecular mechanisms
non-permissive biological barriers
obligate intracellular parasite
oral infection
proMMP-9 secretion
T. gondii
THP-1 cells
various basal membranes
wide range