J Antimicrob Chemother 2005, 56:879–886 PubMedCrossRef Competing

J Antimicrob Chemother 2005, 56:879–886.PubMedCrossRef Competing interests The authors have no competing interests to declare.

Authors’ contributions https://www.selleckchem.com/products/ars-1620.html LL conceived the study design and coordinated the study, carried out the microdilution methods, performed the statistical analysis and drafted the manuscript. DCP carried out the microdilution methods, performed the statistical analysis and drafted the manuscript. RMP participated in the design of the study and drafted the manuscript. APZ analysed and drafted the manuscript. ALB conceived the study design, coordinated the study and drafted the manuscript. All authors read and approved the final manuscript.”
“Background Multiple

studies demonstrate that non coding RNAs (or small RNAs (sRNAs)) possess regulatory roles in the bacterial stress response [1–4]. Bacterial sRNA regulators typically range from 50 – 250 nts and are often transcribed from intergenic regions (IGRs), although open reading frames may also encode sRNAs [5]. Most sRNAs act as regulators at the post-transcriptional level by base-pairing with target mRNAs; these sRNA-mRNA binding regions are often short and imperfect and may require an additional RNA chaperone, which in most cases is the Hfq protein [6, 7]. This imperfect binding allows each sRNA molecule to control multiple targets [8], learn more Staurosporine where either the translation of the target

mRNA is upregulated, or more commonly inhibited. Many sRNA regulators are upregulated when bacteria sense environmental stress: these include oxidative stress [1], low pH environment [2], nutrient deprivation [4] and glucose-phosphate stress [3]. Despite overwhelming evidence that sRNAs play a role when bacteria experience physiological stress, no systematic study has been undertaken to ascertain the impact or levels of sRNA production in bacteria when antibiotics are present. Naturally susceptible pathogens can develop drug resistance when treated with antibiotics [9]. Genetically acquired antibiotic resistance in pathogenic bacteria, via spontaneous / random mutations and horizontal gene transfer, is a significant issue in the treatment of click here infectious diseases [10]. Intrinsic regulatory networks such as those mediated by the transcriptional regulators MarA, SoxS and RamA are also implicated in the development of antibiotic resistance particularly since these systems control the influx / efflux of antibiotics [11]. Thus far studies that have focused on the intrinsic antibiotic resistome are limited to gene and protein networks mediated by these gene operons or other transcription factors [11–13]. Hence the role of the newly uncovered class of regulatory molecules such as sRNAs in controlling or contributing to the antimicrobial resistance phenotype is largely unknown.

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