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Global gene-expression profiles of intracellular survival of the BruAb2_1031 gene mutated Brucella abortus in professional phagocytes, RAW 264.7 cells

Cited 5 time in Web of Science Cited 6 time in Scopus
Authors

Jung, Myunghwan; Shim, Soojin; Im, Young Bin; Park, Woo Bin; Yoo, Han Sang

Issue Date
2018-07-31
Publisher
BioMed Central
Citation
BMC Microbiology, 18(1):82
Keywords
BruAb2_1031 geneIntracellular survivalDefective mutantBrucella abortus
Abstract
Background
Since recognizing the interaction between Brucella and host cells is crucial to the elucidation of the infectious process, Brucella researches have prioritized the investigation of genes related to pathogenicity. To demonstrate the roles of Brucella genes, RAW 264.7 cells were infected with the Brucella abortus wild-type and mutant strains (generated using transposon mutagenesis), after which the different transcriptional responses of the infected cells were determined using microarray.

Results
Following infection, enhanced strategies for intracellular survival, such as down-regulation of genes associated with cytokine responses and apoptosis, were observed in RAW 264.7 cells infected with C3 mutant strain when compared to the transcriptional responses of wild-type infected cells. Using sequence analysis, we determined the mutation site of a C3 mutant strain as the ATP-binding cassette transporter permease (BruAb2_1031). These results were evidenced by an increased level of intracellular survival of the C3 mutant strain.

Conclusions
Characteristics of each mutant strain including bacterial growth rate, abilities to induce cytokine production in macrophages after infection, internalization, and levels of intracellular survival and replication, were investigated by performing RAW 264.7 cell infection experiments. Our results indicate that the BruAb2_1031 gene might be closely related with intracellular survival of B. abortus in RAW 264.7 cells.
ISSN
1471-2180
Language
English
URI
https://hdl.handle.net/10371/143523
DOI
https://doi.org/10.1186/s12866-018-1223-7
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