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DOI 10.1016/j.micpath.2016.04.003

Медицинская библиотека · Microbial pathogenesis · 2016

Evaluation of the tannic acid inhibitory effect against the NorA efflux pump of Staphylococcus aureus.

Tintino Saulo R, Oliveira-Tintino Cícera D M, Campina Fábia F, Silva Raimundo L P, Costa Maria do S, Menezes Irwin R A, Calixto-Júnior João T, Siqueira-Junior José P, Coutinho Henrique D M, Leal-Balbino Tereza C, Balbino Valdir Q

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Аннотация

During the early periods of antibiotic usage, bacterial infections were considered tamed. However, widespread antibiotic use has promoted the emergence of antibiotic-resistant pathogens, including multidrug resistant strains. Active efflux is a mechanism for bacterial resistance to inhibitory substances, known simply as drug efflux pumps. The bacterium Staphylococcus aureus is an important pathogenic bacterium responsible for an array of infections. The NorA efflux pump has been shown to be responsible for moderate fluoroquinolone resistance of S. aureus. The inhibition of the efflux pump was assayed using a sub-inhibitory concentration of standard efflux pump inhibitors and tannic acid (MIC/8), where its capacity to decrease the MIC of Ethidium bromide (EtBr) and antibiotics due to the possible inhibitory effect of these substances was observed. The MICs of EtBr and antibiotics were significantly reduced in the presence of tannic acid, indicating the inhibitory effect of this agent against the efflux pumps of both strains causing a three-fold reduction of the MIC when compared with the control. These results indicate the possible usage of tannic acid as an adjuvant in antibiotic therapy against multidrug resistant bacteria (MDR).

Для цитирования: Tintino Saulo R, Oliveira-Tintino Cícera D M, Campina Fábia F, Silva Raimundo L P, Costa Maria do S, Menezes Irwin R A, Calixto-Júnior João T, Siqueira-Junior José P, Coutinho Henrique D M, Leal-Balbino Tereza C, Balbino Valdir Q. Evaluation of the tannic acid inhibitory effect against the NorA efflux pump of Staphylococcus aureus.. Microbial pathogenesis. 2016. DOI: 10.1016/j.micpath.2016.04.003.

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