Genome-wide transcriptional analysis and other antimicrobials A number

of studies have shown that traditional antibiotics affect bacterial gene expression and physiology [1, 2, 63, 64]. Thus, Idasanutlin some β-lactam antibiotics that can also inhibit peptidoglycan synthesis have been shown to induce the production of colanic acid in E. coli, which indicates that these might exacerbate biofilm formation [65]. Investigation of the E. coli transcription profile in response to bactericidal SAHA solubility dmso concentrations of ampicillin also showed induction of the colanic acid biosynthetic pathway, as well as rcsA, the transcriptional activator of colanic acid synthesis and other stress responses [66]. However, the authors did not detect induction of the additional exopolysaccharide

operon yjbEFGH, distinct from colanic acid. In Staphylococcus aureus, subinhibitory concentrations of β-lactams have been shown to up-regulate some virulence genes [67]. Moreover, the aminoglycoside tobramycin has been shown to induce biofilm formation in E. coli and in Pseudomonas aeruginosa, due to alterations in the levels of c-di-GMP [68]. Biofilm formation was also induced following exposure of P. aeruginosa to subinhibitory concentrations selleck chemical of tetracycline and norfloxacin [69]. Further to this, a number of studies have investigated the effects of antibiotics on the expression of the SOS regulon genes. Thus, the β-lactam antibiotic, ceftazidime, which is an inhibitor of a protein involved in cell wall biosynthesis, PBP3, has been shown to induce transcription of the dinB gene, which encodes the error-prone DNA polymerase Pol IV [70]. Subsequently, subinhibitory concentrations of ampicillin, norfloxacin and kanamycin were shown to induce mutagenesis due to antibiotic-mediated increases in reactive oxygen species, which results in SOS-induced mutagenesis that might lead to multidrug resistance Protirelin [71]. An additional study showed that a number of antibiotics can promote

an increase in mutation frequency; namely, ampicillin, ceftazidime, imipenem, ciprofloxacin, trimethoprim, sulfamethoxazole and tetracycline [72]. With the exception of imipenem, fosfomycin and tetracycline, the antibiotics tested were shown to induce recA expression, while inactivation of recA abolished the mutagenic effects. In the present study, subinhibitory concentrations of colicin M did not induce the expression of dinB or recA. To further confirm that colicin M does not induce the SOS response, induction of the sulA gene following colicin M treatment was investigated. SOS-regulated SulA inhibits cell division by binding to FtsZ, which is required for septum formation. For this purpose, expression of the chromosomal sulA-lacZ fusion was studied in the ENZ1257 strain [73] without and with colicin M: no induction was detected (data not shown).