RNA-Seq-based transcriptome analysis of methicillin-resistant Staphylococcus aureus growth inhibition by propionate

is a pathogen that causes a variety of infectious diseases such as pneumonia, endocarditis, and septic shock. Methicillin-resistant (MRSA) evades virtually all available treatments, creating the need for an alternative control strategy. Although we previously demonstrated the inhibitory effect of so...

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Published inFrontiers in microbiology Vol. 13; p. 1063650
Main Authors Im, Jintaek, Lee, Dongwook, Park, Ok-Jin, Natarajan, Sathishkumar, Park, Junhyung, Yun, Cheol-Heui, Han, Seung Hyun
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 22.12.2022
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Summary:is a pathogen that causes a variety of infectious diseases such as pneumonia, endocarditis, and septic shock. Methicillin-resistant (MRSA) evades virtually all available treatments, creating the need for an alternative control strategy. Although we previously demonstrated the inhibitory effect of sodium propionate (NaP) on MRSA, the regulatory mechanism of this effect remains unclear. In this study, we investigated the regulatory mechanism responsible for the inhibitory effect of NaP on MRSA using RNA-Seq analysis. Total RNAs were isolated from non-treated and 50 mM NaP-treated S. aureus USA300 for 3 h and transcriptional profiling was conducted by RNA-Seq analysis. A total of 171 differentially expressed genes (DEGs) with log fold change ≥2 and < 0.05 was identified in the NaP treatment group compared with the control group. Among the 171 genes, 131 were up-regulated and 40 were down-regulated. Upon gene ontology (GO) annotation analysis, total 26 specific GO terms in "Biological process," "Molecular function," and "Cellular component" were identified in MRSA treated with NaP for 3 h. "Purine metabolism"; "riboflavin metabolism"; and "glycine, serine, and threonine metabolism" were identified as major altered metabolic pathways among the eight significantly enriched KEGG pathways in MRSA treated with NaP. Furthermore, the MRSA strains deficient in , , , or , which were the up-regulated DEGs in the metabolic pathways, were more susceptible to NaP than wild-type MRSA. Collectively, these results demonstrate that NaP attenuates MRSA growth by altering its metabolic pathways, suggesting that NaP can be used as a potential bacteriostatic agent for prevention of MRSA infection.
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Edited by: Michal Letek, Universidad de León, Spain
This article was submitted to Infectious Agents and Disease, a section of the journal Frontiers in Microbiology
Reviewed by: Heather Bennett Miller, High Point University, United States; Volker Behrends, University of Roehampton London, United Kingdom; Jie Hui, Harvard Medical School, United States
ISSN:1664-302X
1664-302X
DOI:10.3389/fmicb.2022.1063650