Profiling of gene expression in methicillin-resistant Staphylococcus aureus in response to cyclo -( l -Val- l -Pro) and
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ORIGINAL PAPER
Profiling of gene expression in methicillin‑resistant Staphylococcus aureus in response to cyclo‑(l‑Val‑l‑Pro) and chloramphenicol isolated from Streptomyces sp., SUK 25 reveals gene downregulation in multiple biological targets Noraziah M. Zin1 · Muhanna M. Al‑shaibani1 · Juriyati Jalil2 · Asif Sukri1 · Anis Rageh Al‑Maleki3,4 · Nik Marzuki Sidik5 Received: 12 October 2019 / Revised: 8 April 2020 / Accepted: 11 May 2020 © Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Chloramphenicol (CAP) and cyclo-(l-Val-l-Pro) were previously isolated from Streptomyces sp., SUK 25 which exhibited a high potency against methicillin-resistant Staphylococcus aureus (MRSA). This study aimed to profile gene expression of MRSA treated with CAP and cyclo-(l-Val-l-Pro) compounds using DNA microarray. Treatment of MRSA with CAP resulted in upregulation of genes involved in protein synthesis, suggesting the coping mechanism of MRSA due to the inhibition of protein synthesis effect from CAP. Most upregulated genes in cyclo-(l-Val-l-Pro) were putative genes with unknown functions. Interestingly, genes encoding ribosomal proteins, cell membrane synthesis, DNA metabolism, citric acid cycle and virulence were downregulated in MRSA treated with cyclo-(l-Val-l-Pro) compound, suggesting the efficacy of this compound in targeting multiple biological pathways. Contrary to CAP, with only a single target, cyclo-(l-Val-l-Pro) isolated from this study had multiple antimicrobial targets that can delay antibiotic resistance and hence is a potential antimicrobial agent of MRSA. Keywords Chloramphenicol · Cyclo-(l-val-l-pro) · Streptomyces SUK 25 · MRSA · DNA microarray Communicated by Erko Stackebrandt.
Introduction
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00203-020-01896-x) contains supplementary material, which is available to authorized users.
The first methicillin-resistant S. aureus (MRSA) was discovered in 1961, after introduced to patients less than a year (Harkins et al. 2017; Jevons et al. 1961). MRSA is a nosocomial and community-acquired pathogen (Maltezou and Giamarellou 2006) that has caused endemic and epidemic nosocomial infections in many parts of the world (Klein et al. 2007; Streulens et al. 1992). In fact, the increased cases of MRSA reported in hospitals might have been due to increased transmission of strains among inpatients and admission of patients previously colonized at other hospitals (David and Daum 2010; Ishak et al. 2016; Tacconelli 2008). The MRSA is cross-resistant to all currently licensed β-lactam antibiotic (Nathwani et al. 2008; Rayner and Munckhof 2005), with resistance to methicillin also associated with resistance to all penicillins and cephalosporins (Chambers and DeLeo 2009). Production of betalactamase encoded by a blaZ gene deactivates penicillin by β-lactam ring hydrolysis. The resistance of the mecA gene
* Muhanna M. Al‑shaibani [email protected] * Nik Marzuki Sidik [email protected] 1
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