Toll-like receptors (TLRs) are key components of the innate immune system that trigger antimicrobial host defense responses. The aim of the present study was to analyze the effects of probiotic Escherichia coli Nissle strain 1917 in experimental colitis induced in TLR-2 and TLR-4 knockout mice. Colitis was induced in wild-type (wt), TLR-2 knockout, and TLR-4 knockout mice via administration of 5% dextran sodium sulfate (DSS). Mice were treated with either 0.9% NaCl or 10 7 E. coli Nissle 1917 twice daily, followed by the determination of disease activity, mucosal damage, and cytokine secretion. wt and TLR-2 knockout mice exposed to DSS developed acute colitis, whereas TLR-4 knockout mice developed significantly less inflammation. In wt mice, but not TLR-2 or TLR-4 knockout mice, E. coli Nissle 1917 ameliorated colitis and decreased proinflammatory cytokine secretion. In TLR-2 knockout mice a selective reduction of gamma interferon secretion was observed after E. coli Nissle 1917 treatment. In TLR-4 knockout mice, cytokine secretion was almost undetectable and not modulated by E. coli Nissle 1917, indicating that TLR-4 knockout mice do not develop colitis similar to the wt mice. Coculture of E. coli Nissle 1917 and human T cells increased TLR-2 and TLR-4 protein expression in T cells and increased NF-B activity via TLR-2 and TLR-4. In conclusion, our data provide evidence that E. coli Nissle 1917 ameliorates experimental induced colitis in mice via TLR-2-and TLR-4-dependent pathways.

Normal values and upper limits (95th percentile) of liver, spleen, pancreas, and portal vein size were determined prospectively with ultrasound in 915 healthy subjects. Sex, age, weight, height, and body surface area were determined in each case. Since correlation of longitudinal and transverse organ diameters with physical data was poor (r less than or equal to 0.3), the authors do not consider it necessary to correct the measurements accordingly. However, the liver is oriented longitudinally in slender subjects and transversely in heavy subjects; thus both longitudinal and anteroposterior diameters need to be measured, since the longitudinal diameter alone will give too high or too low a value, respectively.

DRKS00007768; Pre-results.

SUMMARY Previous investigations of stress effects on gastric emptying, orocaecal, and colonic transit in rats have produced conflicting results. Here one type of stressor, a 'passive avoidance' situation, was used to investigate its effects on gastric emptying, orocaecal and colonic transit. After the rats had been trained to eat a standard amount of semisolid food, gastric emptying was determined (n=12) by the food remaining in the stomach after various periods of rest, or stress exposure. Orocaecal transit (n=14) was determined by breath hydrogen measurements after the food had been labelled with 1 g lactose. Colonic transit (n=18) was measured as the arrival time of coloured faeces after infusion of a carmine red solution into the caecum through a chronically implanted catheter. The stressor had differential effects on transit through the stomach, small bowel and colon: gastric emptying was delayed (p<005) after stress (t/2=2.66 h after stress, 1.97 h at rest). Orocaecal transit was accelerated (p<005) after stress; transit time decreased from 124.3 min at rest to 86-2 min after stress. Colonic transit was accelerated (p<001) under stress, from 15X5 h to 1X29 h. It is concluded that gastrointestinal transit in different parts of the gastrointestinal tract is differently affected by central nervous stimuli.