1,720,992 research outputs found
Lipoteichoic acid and protein-A from Staphylococcus aureus stimulate release of hepatocyte growth factor (HGF) by human dermal fibroblasts
No full textTopical amikacin formulation induces fibroblast growth factor and cytokine release from human dermal fibroblasts
No full textMALASSEZIA FURFUR INVASIVINESS IN A KERATINOCYTES CELL LINE (HACAT): EFFECTS ON CYTOSKELETON AND ON ADHESION MOLECULES AND CYTOKINE EXPRESSION
No full textLactoferrin downregulates pro-inflammatory cytokines upexpressed in intestinal epithelial cells infected with invasive or noninvasive Escherichia coli strains
No full textIntestinal epithelial cells are able to differentially interact with commensal or pathogenic microorganisms, triggering a physiological or destructive inflammation, respectively. To mimic commensal-enteroinvasive bacteria-host cell interaction, we infected Caco-2 cells with noninvasive Escherichia coli HB101 and with recombinant invasive E. coli HB101(pRI203). Using DNA microarray mRNA profiling and ELISA assays, we studied the expression of several cytokine and cytokine-related genes in infected Caco-2 cells in the absence or presence of bovine lactoferrin (bLf). Infection of Caco-2 cells with the noninvasive strain induced a slight increase in the expression of interleukin 8 (IL-8), whereas infection with invasive E. coli HB101(pRI203) induced a significant increase in the expression of IL-8 as well as other pro-inflammatory cytokines. The addition of bLf, in native- or holo-form, did not influence expression of cytokine genes by uninfected Caco-2 cells, but it decreased expression of IL-8 by cells infected with E.coli HB101. Moreover, except for IL-8, bLfs dramatically downregulated pro-inflammatory cytokines upexpressed by Caco-2 cells infected with the invasive strain. Although IL-8 was decreased by bLfs, it remained upregulated, suggesting that it could be a signal of persistence of intracellular bacteria. The bLf ability to reduce expression of some pro-inflammatory cytokines, which appears independent of its iron saturation, might represent an important natural mechanism in regulating epithelial cell responses to pathogenic bacteria and in limiting cell damage and the spread of infections
Meccanismo di regolazione dell’espressione di Metalloproteasi-2 in risposta al nichel solfato in cheratinocit umani
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PORIN FROM P.AERUGINOSA INDUCE APOPTOSIS IN AN EPITHELIAL CELL LINE DERIVED FROM RAT SEMINAL VESCICLES
No full textRuolo delle metallo proteasi di matrice nella dermatite allergica da contatto di tipo professionale
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