SummaryOne of the promising approaches in the therapy of ulcerative colitis is administration of butyrate, an energy source for colonocytes, into the lumen of the colon. This study investigates the effect of butyrate producing bacterium Clostridium tyrobutyricum on dextran sodium sulphate (

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Organisms live in continuos interaction with their environment; this interaction is of vital importance but at the same time can be life threatening. The largest and most important interface between the organism and its environment is represented by surfaces covered with epithelial cells. Of these surfaces, mucosae comprise in humans approximately 300 m 2 , and the skin covers approximately 1.8 m 2 surface of the human body. Mucosal tissues contain two effector arms of the immune system, innate and adaptive, which operate in synergy. Interaction with commensal bacteria, which outnumber the nucleated cells of our body, occurs physiologically on epithelial surfaces; this interaction could pose the risk of inflammation. The mucosal immune system has developed a complex network of regulatory signalling cascades that is a prerequisite for proper activation but also for a timely inactivation of the pathway. As demonstrated in gnotobiotic animal models of human diseases, impaired regulation of mucosal responses to commensal bacteria plays an important role in the development of several inflammatory and autoimmune diseases.

1. The aerobic accumulation of various monosaccharides in slices of rabbit kidney cortex at 25 degrees was studied. 2. d-Fructose and alpha-methyl d-glucoside were readily accumulated against their concentration gradient by a phlorrhizin-sensitive Na(+)-dependent active transport. In the absence of external Na(+) the maximal rate of alpha-methyl glucoside transport was decreased tenfold, the K(m) of entry into the cells (8.2mm) not being affected. Phlorrhizin and d-galactose inhibited the entry of alpha-methyl glucoside also in the absence of external Na(+). 3. d-Xylose, 6-deoxy-d-glucose and 6-deoxy-d-galactose were poorly accumulated ([S](i)/[S](o) ratios slightly above 1.0); this transport was inhibited by phlorrhizin and by the absence of Na(+). 4. 3-O-Methyl-d-glucose, d-arabinose and l-arabinose were not actively transported, [S](i)/[S](o) ratios never exceeding 1.0. 5. 2-Deoxy-d-glucose and 2-deoxy-d-galactose were readily accumulated against a high concentration gradient, this transport being Na(+)-independent and only slightly sensitive to phlorrhizin. External Na(+) was not required for an inhibitory action of phlorrhizin and d-galactose on the entry of 2-deoxy-d-galactose into the cells. 6. Interference for entry into the cells between the following saccharides was found: d-galactose inhibited alpha-methyl d-glucoside transport; d-xylose entry was inhibited by d-glucose; d-galactose transport was inhibited by d-xylose; a mutual interference between d-galactose and its 2-deoxy analogue was found. 7. It is concluded that d-glucose, d-galactose, alpha-methyl d-glucoside, d-xylose and possibly also some other monosaccharides share a common active transport system. 8. The specificity of the Na(+)-dependent phlorrhizin-sensitive active transport system for monosaccharides in kidney-cortex cells differs from that in intestinal epithelial cells.

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The multifunctional cytokine interleukin-18 (IL-18) is an important mediator in intestinal inflammatory processes. The aim of this study was to evaluate the constitutive expression of IL-18 and its receptors (IL-18R␣ and IL-18R␤) in intestinal epithelial cells (IEC) stimulated by tumor necrosis factor-␣ (TNF-␣) and interferon-␥ (IFN-␥). In addition, cellular proliferation and evaluation of brush border enzymes as differentiation markers were studied. Nontransformed rat intestinal epithelial IEC-6 cells were grown on an extracellular matrix (ECM) in medium with or without TNF-␣, IFN-␥, or a combination of both. Gene expression of IL-18, its receptors and apoptotic markers was evaluated using real-time PCR. Expression of IL-18R␣ protein was demonstrated by flow cytometry and Western blot. Enzymatic activities of brush border enzymes and caspase-1 were determined. The constitutive expression of IL-18, IL-18R␣ and IL-18R␤ mRNAs and proteinswere detected in IEC-6 cells. The biologically active form of IL-18 was released in response to TNF-␣ and IFN-␥ treatment. Exogenous IL-18 had no effect on cellular proliferation, brush border enzyme activities, and gene expression of apoptotic markers. However, the addition of IL-18 stimulated production and release of the chemokine IL-8. These data suggest that IEC-6 cells may be not only a source of IL-18 but also a target for its action. 287