Burkholderia pseudomallei capsule exacerbates respiratory melioidosis but does not afford protection against antimicrobial signaling or bacterial killing in human olfactory ensheathing cells

Dando, Samantha J., Ipe, Deepak S., Batzloff, Michael, Sullivan, Matthew J., Crossman, David K., Crowley, Michael, Strong, Emily, Kyan, Stephanie, Leclercq, Sophie Y., Ekberg, Jenny A. K., St John, James, Beacham, Ifor R. and Ulett, Glen C. (2016) Burkholderia pseudomallei capsule exacerbates respiratory melioidosis but does not afford protection against antimicrobial signaling or bacterial killing in human olfactory ensheathing cells. Infection and Immunity, 84 7: 1941-1956. doi:10.1128/IAI.01546-15

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Author Dando, Samantha J.
Ipe, Deepak S.
Batzloff, Michael
Sullivan, Matthew J.
Crossman, David K.
Crowley, Michael
Strong, Emily
Kyan, Stephanie
Leclercq, Sophie Y.
Ekberg, Jenny A. K.
St John, James
Beacham, Ifor R.
Ulett, Glen C.
Title Burkholderia pseudomallei capsule exacerbates respiratory melioidosis but does not afford protection against antimicrobial signaling or bacterial killing in human olfactory ensheathing cells
Formatted title
Burkholderia pseudomallei capsule exacerbates respiratory melioidosis but does not afford protection against antimicrobial signaling or bacterial killing in human olfactory ensheathing cells
Journal name Infection and Immunity   Check publisher's open access policy
ISSN 1098-5522
1070-6313
0019-9567
Publication date 2016-07
Year available 2016
Sub-type Article (original research)
DOI 10.1128/IAI.01546-15
Open Access Status File (Publisher version)
Volume 84
Issue 7
Start page 1941
End page 1956
Total pages 16
Place of publication Washington, DC, United States
Publisher American Society for Microbiology
Collection year 2017
Language eng
Formatted abstract
Melioidosis, caused by the bacterium Burkholderia pseudomallei, is an often severe infection that regularly involves respiratory disease following inhalation exposure. Intranasal (i.n.) inoculation of mice represents an experimental approach used to study the contributions of bacterial capsular polysaccharide I (CPS I) to virulence during acute disease. We used aerosol delivery of B. pseudomallei to establish respiratory infection in mice and studied CPS I in the context of innate immune responses. CPS I improved B. pseudomallei survival in vivo and triggered multiple cytokine responses, neutrophil infiltration, and acute inflammatory histopathology in the spleen, liver, nasal-associated lymphoid tissue, and olfactory mucosa (OM). To further explore the role of the OM response to B. pseudomallei infection, we infected human olfactory ensheathing cells (OECs) in vitro and measured bacterial invasion and the cytokine responses induced following infection. Human OECs killed >90% of the B. pseudomallei in a CPS I-independent manner and exhibited an antibacterial cytokine response comprising granulocyte colony-stimulating factor, tumor necrosis factor alpha, and several regulatory cytokines. In-depth genome-wide transcriptomic profiling of the OEC response by RNA-Seq revealed a network of signaling pathways activated in OECs following infection involving a novel group of 378 genes that encode biological pathways controlling cellular movement, inflammation, immunological disease, and molecular transport. This represents the first antimicrobial program to be described in human OECs and establishes the extensive transcriptional defense network accessible in these cells. Collectively, these findings show a role for CPS I in B. pseudomallei survival in vivo following inhalation infection and the antibacterial signaling network that exists in human OM and OECs.
Keyword Burkholderia pseudomallei
Infection
Bacterial capsular polysaccharide I (CPS I)
Olfactory mucosa (OM)
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: HERDC Pre-Audit
School of Chemistry and Molecular Biosciences
 
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