作者: Thuy Do Thi , Elena López , Alexandro Rodríguez-Rojas , Jerónimo Rodríguez-Beltrán , Alejandro Couce
DOI: 10.1093/JAC/DKQ496
关键词:
摘要: Objectives: Low concentrations of some antibiotics have been reported to stimulate mutagenesis and recombination, which may facilitate bacterial adaptation different types stress, including antibiotic pressure. However, the mutagenic effect most currently used remains untested. Furthermore, it is known that in many bacteria, Escherichia coli, stimulation mediated by SOS response. Thus, blockage or attenuation this response through inhibition RecA has proposed as a possible therapeutic adjuvant combined therapy reduce ability generate antibiotic-resistant mutants. The aim work was study capacity sublethal antimicrobials families with molecular targets increase mutant frequency E. inactivation recA would on antibiotic-mediated mutagenesis. Methods: We tested mutagenicity following antimicrobials: ampicillin; ceftazidime; imipenem; fosfomycin; ciprofloxacin; trimethoprim; sulfamethoxazole; trimethoprim/sulfamethoxazole; colistin; tetracycline; gentamicin; rifampicin; chloramphenicol. Results: Eight out 13 coli (slightly cases), trimethoprim, alone combination sulfamethoxazole, producing highest effect. Inactivation abolishes also produces increased susceptibility antimicrobials. Conclusions: fact reduces and/or increases activity large number supports hypothesis might favourable effects therapy.