Abstract
Several genes involved in the determination of Listeria monocytogenes pathogenesis have been identified. Among them, plcA gene encodes phosphatidylinositol-specific phospholipase C (PI-PLC), plcB gene encodes a broad-range phospholipase C (PC-PLC), and acta encodes a protein contributing to actin assembly in infected cells. The interaction of L. monocytogenes wild type (LO 28) strain and two derivative mutants, plcA- (BUG 206) and actA- /plcB- (LUT 12), with macrophages and T lymphocytes was investigated in a mouse model of listeriosis. Both mutants showed evidence of attenuation. The plcA mutant, but not the plcB- mutant, expressed an increase in susceptibility to the anti-listerial activity of macrophages. Both mutants showed a decreased ability to induce IL-12 production by bone marrow macrophages when co-stimulated with E. coli LPS or IFN-γ. In vivo, L monocytogenes plcA mutant was found to be a more effective stimulator of T cells than the wild LO 28 strain.
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Rudnicka, W., Kaczmarek, M., Szeliga, J., Germann, T., Wieckowska, M., & Rózalska, B. (1997). The host response to listeria monocytogenes mutants defective in genes encoding phospholipases C (plcA, plcB) and actin assembly (actA). Microbiology and Immunology, 41(11), 847–853. https://doi.org/10.1111/j.1348-0421.1997.tb01939.x
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