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Dynamics of the Listeria monocytogenes infection monitored by phospholipid fatty acids in the liver of BALB/C mice

The liver is major target organ for the experimental Listeria monocytogenes infection. Hepatocytes are the principal cell type harbouring the replicating bacterial pathogen within the liver until the infection is controlled by cell mediated immunity. The consequences are hepatic inflammation as well as alteration of membrane fluidity and changes of cellular functions such as carrier-mediated transport, phagocytosis, endocytosis, immunologic cytotoxicity, prostaglandin production. In an experimental model of murine listeriosis we monitored histopathological and biochemical changes in the liver tissue. Infected mice were sacrificed on days 1, 3 and 6 after infection and sera and livers were collected. The course of infection was monitored using bacteriological, histological and biochemical methods. Dynamics of the liver phospholipid fatty acids (PLFAs) were determined by gas chromatography following isolation and purification by solid-phase-extraction using an aminopropylsilica column. All infected animals exhibited severe patohistological changes and metabolic dysfunctions according to high levels of serum aminotransferases. Significant differences in the PLFAs were found. The markedly reduced polyunsaturated FA at the first day may reflect suppression of immunity in the beginning of infection. Reduced monounsaturated FA reveals reduction in membrane fluidity. Ratio of the n-3 and n-6 FAs families was significantly elevated which led to lower production of eicosanoids of the 2-series. The desaturase activity was altered: the D9 C18 and D5D desaturation index were significantly decreased, the D6D was increased, while D9 C16 desaturation index was not affected. Current understanding based on the found PLFAs composition changes may give better insight in the pathogenesis of listeria infection.

Listeria monocytogenes; mice; liver; phospholipid fatty acids

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