Publications by authors named "M H Coconnier"

In the present study, the role of direct procaryote-eucaryote interactions in the virulence of Bacillus cereus was investigated. As a model of human enterocytes, differentiated Caco-2 cells were used. Infection of fully differentiated Caco-2 cells with B.

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Probiotic lactic acid strains are live micro-organisms that, when consumed in adequate amounts as part of food, confer a health benefit on the host. The scientific basis for the use of selected probiotic strains has only recently been firmly established, and appropriate and well-conducted experimental in vitro and in vivo studies, as well as clinical studies, are now beginning to be published, especially with regard to the effectiveness of probiotic strains in antagonizing pathogens. In particular, experimental data have allowed new insights into selected probiotic strains that express strain-specific probiotic properties and into the mechanism of action of these strains.

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The secreted thiol-activated cytolysin listeriolysin O (LLO) was responsible for L. monocytogenes-induced high-molecular glycoproteins (HMGs) exocytosis in cultured human mucosecreting HT29-MTX cells. By biochemical analysis we demonstrate that the majority of secreted HMGs in LLO-stimulated cells are of mucin origin.

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Background And Aims: The normal gastrointestinal microflora exerts a barrier effect against enteropathogens. The aim of this study was to examine whether lactobacilli, a minor genus of the resident gut microflora, exerts a protective effect against the cellular injuries promoted by the diarrhoeagenic Afa/Dr diffusely adhering Escherichia coli (Afa/Dr DAEC) C1845 strain in human intestinal cells.

Methods: Cultured human intestinal fully differentiated enterocyte-like Caco-2/TC7 cells were used.

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Lysteriolysin O (LLO) induces a microtubule-dependent activation of mucin exocytosis in the human mucin-secreting HT29-MTX. Cholesterol inhibits the LLO-induced mucin exocytosis, whereas the oxidized form of cholesterol had no inhibitory effect. LLO-induced mucin exocytosis inhibited by cholesterol can be restored by enzymatic treatment with cholesterol oxidase.

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