BACKGROUND: Yersinia enterocolitica is an important cause of diarrhea, but little is known about the underlying mechanisms. We therefore studied the impact of acute Y. enterocolitica infection on intestinal barrier function in a mouse model. METHODS: For this purpose CD-1 mice were infected with Y. enterocolitica (serotype 08; 6 x 10(7) viable bacteria), and alternating current impedance analysis was performed on days 1, 2, 3, 5, and 8 after infection. RESULTS: The infection resulted in a decrease in epithelial resistance from 18.0 +/- 0.9 omega.cm2 (controls) to 12.1 +/- 0.5 omega.cm2 (day 1, p < 0.001), from which the animals recovered by day 5. To locate this loss in barrier function, the horizontal distribution of local conductances was measured by voltage scanning, yielding two results. First, conductance was homogeneously distributed across the chamber area, excluding erosions or ulcers among the gross surface area and favoring tight junction opening as the source of barrier dysfunction. Second, the conductance of villus tips was compared with that of the intervillus region (consisting of lateral villus walls plus crypts). On day 1 the former was increased by 74% and the latter by 18%. Then, two other mechanisms of diarrhea were tested, namely malabsorption and secretion. First, the increase in ISC after the addition of 3-O-methylglucose, representing Na(+)-glucose cotransport, was shown not to be impaired. Second, bumetanide-inhibitable ISC, representing electrogenic Cl- secretion, also did not differ between controls and infected animals. CONCLUSIONS: Our data show that epithelial barrier dysfunction plays a role in Y. enterocolitica infection, while Na(+)-glucose cotransport and electrogenic Cl- secretion are unaltered.
BACKGROUND:Yersinia enterocolitica is an important cause of diarrhea, but little is known about the underlying mechanisms. We therefore studied the impact of acute Y. enterocolitica infection on intestinal barrier function in a mouse model. METHODS: For this purpose CD-1mice were infected with Y. enterocolitica (serotype 08; 6 x 10(7) viable bacteria), and alternating current impedance analysis was performed on days 1, 2, 3, 5, and 8 after infection. RESULTS: The infection resulted in a decrease in epithelial resistance from 18.0 +/- 0.9 omega.cm2 (controls) to 12.1 +/- 0.5 omega.cm2 (day 1, p < 0.001), from which the animals recovered by day 5. To locate this loss in barrier function, the horizontal distribution of local conductances was measured by voltage scanning, yielding two results. First, conductance was homogeneously distributed across the chamber area, excluding erosions or ulcers among the gross surface area and favoring tight junction opening as the source of barrier dysfunction. Second, the conductance of villus tips was compared with that of the intervillus region (consisting of lateral villus walls plus crypts). On day 1 the former was increased by 74% and the latter by 18%. Then, two other mechanisms of diarrhea were tested, namely malabsorption and secretion. First, the increase in ISC after the addition of 3-O-methylglucose, representing Na(+)-glucose cotransport, was shown not to be impaired. Second, bumetanide-inhibitable ISC, representing electrogenic Cl- secretion, also did not differ between controls and infected animals. CONCLUSIONS: Our data show that epithelial barrier dysfunction plays a role in Y. enterocolitica infection, while Na(+)-glucose cotransport and electrogenic Cl- secretion are unaltered.