The HtrA stress response protease contributes to resistance of Brucella abortus to killing by murine phagocytes

• Published in: Infection and Immunity Vol. 64; no. 11; pp. 4838 - 4841
• Main Authors: Elzer, P.H. (Louisiana State University Agricultural Center, Baton Rouge.), Phillips, R.W, Robertson, G.T, Roop, R.M. II
• Format: Journal Article
• Language: English
• Published: Washington, DC American Society for Microbiology 01-11-1996
• Subjects: Animals; Bacterial Proteins - genetics; Bacterial Proteins - metabolism; Bacteriology; Biological and medical sciences; BRUCELLA ABORTUS; Brucella abortus - enzymology; Brucella abortus - genetics; Brucella abortus - immunology; Brucella abortus - pathogenicity; Brucellosis - immunology; Brucellosis - microbiology; Cells, Cultured; Fundamental and applied biological sciences. Psychology; Heat-Shock Proteins; Macrophages - immunology; Mice; Mice, Inbred BALB C; Microbiology; Mutation; Neutrophils - immunology; Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains; Periplasmic Proteins; Phagocytes - immunology; Serine Endopeptidases - genetics; Serine Endopeptidases - metabolism; Virulence; Pathogenesis; Virulence; Rodentia; Host agent relation; Brucella abortus; Bactericidal effect; Resistance; Vertebrata; Mammalia; Brucellaceae; Mouse; Bacteria; Mutation; Neutrophil; Macrophage; Phagocyte
• ISSN: 0019-9567; 1098-5522
• DOI: 10.1128/IAI.64.11.4838-4841.1996

Compared with virulent Brucella abortus 2308, the isogenic htrA mutant PHE1 shows decreased resistance to killing by cultured murine neutrophils and macrophages and significant attenuation during the early stages of infection in the BALB/c mouse model. These findings further define the contributions of the htrA gene product to the pathogenesis of B. abortus infections