The role of a Brucella abortus lipoprotein in intracellular replication and pathogenicity in experimentally infected mice

• Published in: Microbial pathogenesis 2013-01, Vol.54, p.34-39
• Main Authors: Kim, Dong Hyeok, Son, Byeong Guk, Lim, Jeong Ju, Lee, Jin Ju, Kim, Dae Geun, Lee, Hu Jang, Min, Wongi, Rhee, Man Hee, Kim, Kwang Dong, Chang, Hong Hee, Kim, Suk
• Format: Article
• Language: English
• Subjects: Animals; Bacterial Load; Bacteriology; Biological and medical sciences; Brucella abortus; Brucella abortus - growth & development; Brucella abortus - pathogenicity; Brucella melitensis biovar Abortus; brucellosis; Brucellosis - microbiology; Brucellosis - pathology; Cell Line; Disease Models, Animal; endosomes; Epithelial Cells - microbiology; Female; Fundamental and applied biological sciences. Psychology; gene banks; Gene Deletion; Humans; Lipoprotein; lipoproteins; Lipoproteins - genetics; Lipoproteins - metabolism; live vaccines; lysosomes; macrophages; Macrophages - microbiology; Mice; Mice, Inbred BALB C; Microbiology; Miscellaneous; mutants; Pathogenicity; Phagocyte; spleen; Spleen - microbiology; Virulence; Virulence Factors - genetics; Virulence Factors - metabolism
• ISSN: 0882-4010; 1096-1208
• DOI: 10.1016/j.micpath.2012.09.002

Brucella abortus, the causative agent of brucellosis, can survive and replicate within host cells. Understanding bacterial virulence factors and bacteria-host cell interactions is critical for controlling brucellosis. However, little is known regarding the pathogenic mechanisms of brucellosis. A lipoprotein mutant (Gene Bank ID: 3339351) of B. abortus showed a lower rate of intracellular replication than did the wild-type strain in HeLa cells and RAW 264.7 macrophages. The adherent activity of the lipoprotein mutant was slightly increased compared to that of the wild-type strain in HeLa cells. After infection into macrophages, the lipoprotein mutant co-localized with either late endosomes or lysosomes. In mice infected with the lipoprotein mutant, fewer lipoprotein mutants were recovered from the spleen at 8 weeks post-infection compared to the wild-type strain. The ability to protect the lipoprotein mutant against infection by the virulent B. abortus strain 544 was similar to that of strain RB51. Our results indicate that the B. abortus lipoprotein is an important factor for survival within phagocytes and mice, and the B. abortus lipoprotein mutant may help improve live vaccines used to control brucellosis. ► Brucella abortus lipoprotein mutant did not replicate within phagocytes. ► The lipoprotein mutant showed different phagocytic pathway from that of wild-type. ► The virulence of lipoprotein mutant was lower than that of wild-type in mouse. ► The lipoprotein mutant induces protective immunity against B. abortus 544 in mice.