Unknown,Transcriptomics,Genomics,Proteomics

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Inhibition of Staphylococcus aureus biofilm formation by gurmarin, a plant-derived cyclic peptide

ABSTRACT: Staphylococcus aureus is an opportunistic pathogen capable of causing various infections ranging from superficial skin infections to life-threatening severe diseases, including pneumonia and sepsis. This bacterium is attached to biotic and abiotic surfaces and forms biofilms that are resistant to conventional antimicrobial agents and clearance by host defenses. Infections associated with biofilms may result in longer hospitalizations, a need for surgery, and may even result in death. Agents that inhibit the formation of biofilms and virulence without affecting bacterial growth to avoid the development of drug resistance could be useful for therapeutic purposes. In this regard, we identified and isolated a small cyclic peptide, gurmarin, from a plant source that inhibited the formation of S. aureus biofilm without affecting the growth rate of the bacterium. We determined the gene expression of S. aureus biofilm treated with gurmarin and compared it to the untreated control biofilms. Differentially expressed genes were identified and their roles in the inhibition of S. aureus biofilms by gurmarin were analyzed.

ORGANISM(S): Staphylococcus aureus

SUBMITTER: Joe Fralick

PROVIDER: E-MTAB-12154 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Long non-coding RNAs (lncRNAs) are transcripts of more than 200 nucleotides that are not translated into functional proteins. Cellular lncRNAs have been shown to act as regulators by interacting with target nucleic acids or proteins and modulating their activities. We investigated the role of RNA1.2, which is one of four major lncRNAs expressed by human cytomegalovirus (HCMV), by comparing the properties of parental virus in vitro with those of deletion mutants lacking either most of the RNA1.2 gene or only the TATA element of the promoter. In comparison with parental virus, these mutants exhibited no growth defects and minimal differences in viral gene expression in human fibroblasts. In contrast, 76 cellular genes were consistently up- or down-regulated by the mutants at both the RNA and protein levels at 72 hours after infection. Differential expression of the gene most highly upregulated by the mutants (Tumor protein p63-regulated gene 1-like protein; TPRG1L) was confirmed at both levels by RT-PCR and immunoblotting. Consistent with the known ability of TPRG1L to upregulate IL-6 expression via NF-κB stimulation, RNA1.2 mutant-infected fibroblasts were observed to upregulate IL-6 in addition to TPRG1L. Comparable surface expression of TNF receptors and responsiveness to TNF-α in cells infected by the parental and mutant viruses indicated that activation of signaling by TNF-α is not involved in upregulation of IL-6 by the mutants. In contrast, inhibition of NF-κB activity and knockdown of TPRG1L expression reduced the extracellular release of IL-6 by RNA1.2 mutant-infected cells, thus demonstrating that upregulation of TPRG1L activates NF-κB. The levels of CCL2 and CXCL1 transcripts were also increased in RNA1.2 mutant-infected cells, further demonstrating the presence of active NF-κB signalling. These results suggest that RNA1.2 plays a role in manipulating intrinsic NF-B-dependent cytokine and chemokine release during HCMV infection , thereby impacting downstream immune responses.

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Inhibition of Staphylococcus aureus biofilm formation by gurmarin, a plant-derived cyclic peptide

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