XXXX Induces Cc-chemokine Ligand 20 in Gut Epithelial Cells.

@entity1 @entity6825 @entity29 @entity1366 @entity16365
BACKGROUND AND AIM: Production of chemokines by intestinal epithelial cells is a key step in the amplification of the destructive immune-inflammatory response in @entity1 with @entity29 [ @entity29 ]. In this study, we examined whether intestinal epithelial cells express macrophage colony-stimulating factor receptor 1 [M-CSFR-1], the functional receptor of @entity6825 [ @entity6825 ], a cytokine that is over-produced in @entity29 and supposed to sustain inflammatory pathways. METHODS: M-CSFR-1 expression was evaluated in intestinal samples of @entity29 @entity1 , controls, and colon epithelial cell lines by real-time polymerase chain reaction [PCR], immunohistochemistry, and western blotting. DLD-1 cells were stimulated with @entity6825 in the presence or absence of MAP kinase inhibitors, chemokine induction was assessed by real-time PCR and enzyme-linked immunosorbent assay [ELISA], and mitogen-activated protein (MAP) kinase activation was monitored by western blotting. The effect of a neutralising @entity6825 antibody on @entity16365 synthesis was tested in ex vivo organ cultures of @entity29 mucosal explants. RESULTS: Enhanced expression of M-CSFR-1 RNA transcripts was seen in inflamed mucosa of @entity29 @entity1 as compared with controls. Immunohistochemical analysis confirmed up-regulation of M-CSFR-1 in @entity29 and showed that both epithelial and lamina propria mononuclear cells expressed this receptor. Stimulation of DLD-1 with @entity6825 increased @entity16365 production through an @entity1366 -dependent mechanism. Consistently, treatment of @entity29 explants with anti- @entity6825 reduced @entity16365 production. CONCLUSIONS: These data show that intestinal epithelial cells are a target of @entity6825 and suggest that this cytokine contributes to mediating the cross-talk between epithelial cells and immune cells in @entity29 .
