Abstract
A proton pump-deleted mutant E. coli, AGI00 A, had greater sensitivity to ampicillin, tetracycline and erythromycin than the wild-type parent E. coli AG100 containing the proton pump. This antibiotic sensitivity was further increased by resistance modifiers such as the Ca2+ channel blocker (±) verapamil (VP) and the calmodulin antagonist promethazine (PMZ). Whereas the newly-synthesized trifluoromethyl-ketone (TF) enhanced the activity of these antibiotics against the wild-type strain, it did not enhance the activity of ampicillin against the proton pump-deleted mutant. These results suggested that TF14 had an inhibitory effect on the proton pump. Elimination of plasmds from another strain of E. coli, K12, was promoted by PMZ and 9-amino-acridine (9-AA), but not by TF14 alone. However, combinations of TF14 with either PMZ or 9-AA enhanced the plasmid elimination capacity of the latter compounds. The combination of TF14, PMZ and VP proved that the Ca2+ channel blocker was not effective by itself. These results collectively suggest that TF14 inhibited the proton pump of E. coli and that it was this pump which, when inhibited by TF14, allowed more PMZ to reach its plasmid elimination target.
Original language | English |
---|---|
Pages (from-to) | 367-372 |
Number of pages | 6 |
Journal | In Vivo |
Volume | Vol. 20 |
Issue number | n.º 3 |
Publication status | Published - May 2006 |
Keywords
- Bacterial transporters
- E. coli
- Multidrug resistance
- Plasmid curing
- Proton pump
- Resistance modifiers
- Trifluoromethyl-ketones
UN Sustainable Development Goals (SDGs)
- SDG 3 - Good Health and Well-Being