Campylobacter jejuniの肝障害性に関する研究

Abstract

Mice orally infected Campylobacter jejuni developed focal infiltrative necrotic lesions in the liver, as determined by both histology and liver function tests. Histopathological feature of the liver, a focal infiltrative necrosis, was seen between days 30 and 60 postinoculation, and it became gradually more profound with time, despite the fact that liver functions of infected mice were most affected at 2 months postinoculation. The capacity of C. jejuni to induce hepatic lesions seemed to be related to that of organisms to persist in the gall bladdar. Hepatic lesions following C. jejuni infection was attributable to the hepatotoxic factor which was isolated from the subcellular components of bacteria by two series of chromatographic separations. This factor was able to induce hepatitis after it was injected intravenously into mice at a dose of 10 μg. Hepatotoxic activity of this factor was confirmed by incubating several doses of this factor with mouse hepatocytes : at low concentrations (＜5 μg/ml) hepatocytes became rounding-up, while at high concentrations (＞20 μg/ml) they exhibited cytolytic changes. Among 20 clinical isolates of C. jejuni, only four strains evoked hepatitis in mice and produced the hepatotoxic factor.