6533b7dafe1ef96bd126d7f8
RESEARCH PRODUCT
The Host Response toListeria monocytogenesMutants Defective in Genes Encoding Phospholipases C(plcA, plcB)and Actin Assembly(actA)
Marzena WięckowskaBarbara RóżalskaWiesława RudnickaTieno GermannJacek SzeligaMałgorzata Kaczmareksubject
LipopolysaccharidesCellular immunityT-LymphocytesImmunologyMutantDose-Response Relationship ImmunologicBiologyLymphocyte ActivationPhosphatidylinositolsmedicine.disease_causeMicrobiologyMicrobiologyMicePhagocytosisListeria monocytogenesVirologyEscherichia colimedicineAnimalsListeriosisGeneEscherichia coliCells CulturedMice Inbred BALB CPhospholipase CWild typeInterleukin-12Listeria monocytogenesActinsGenes BacterialType C PhospholipasesMutationMacrophages PeritonealInterleukin 12FemaleSpleendescription
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-gamma. In vivo, L. monocytogenes plcA- mutant was found to be a more effective stimulator of T cells than the wild LO 28 strain.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 1997-11-01 | Microbiology and Immunology |