The HtrA stress response protease contributes to resistance of Brucella abortus to killing by murine phagocytes.
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.
Department of Microbiology and Immunology, Louisiana State University Medical Center, Shreveport 71130-3932, USA.
P H
PH
Elzer
R W
RW
Phillips
G T
GT
Robertson
R M
RM
Roop
D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism; D002003:Brucella abortus / Q000201:enzymology* / Q000235:genetics / Q000276:immunology* / Q000472:pathogenicity; D002006:Brucellosis / Q000276:immunology* / Q000382:microbiology; D002478:Cells, Cultured; D006360:Heat-Shock Proteins; D008264:Macrophages / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D009154:Mutation; D009504:Neutrophils / Q000276:immunology; D033903:Periplasmic Proteins; D010586:Phagocytes / Q000276:immunology*; D012697:Serine Endopeptidases / Q000235:genetics / Q000378:metabolism*; D014774:Virulence
D001426:Bacterial Proteins; D006360:Heat-Shock Proteins; D033903:Periplasmic Proteins; C061682:DegP protease; D012697:Serine Endopeptidases