The antibiotic resistance among pathogenic bacteria is one of the biggest problems in public health. Bacterial geneticists at the University of Lyon have found that E. coli can synthesize drug-resistant proteins even in the presence of antibiotics. A well-preserved membrane pump removes antibiotics from the cells, allowing long enough time for the cells to receive DNA from neighboring cells that encode a resistance protein.
The researchers used the normal antibiotic resistance gene of E. coli as the research object, and carefully observed how the bacteria encode the TetA protein by DNA (the TetA protein is a pump that makes cells resistant to tetracycline by shunting out tetracycline). They found that after the plasmid DNA reached the non-resistant cells for a period of time, red fluorescence appeared on the receptor cell membrane, indicating that the TetA protein was translated and the cells were resistant to tetracycline.
The researchers then exposed the cells to high concentrations of tetracycline and placed them under the microscope again. They observed that plasmid DNA reached new non-resistant cells. This is expected because tetracycline does not hinder this process. However, it prevents protein production.
But the researchers found red fluorescence in some of the new recipient cells, which previously had no TetA protein. Obviously, despite exposure to tetracycline, they are still able to synthesize proteins, including TetA.
The researchers found that the AcrAB-TolC pump can prolong the survival of bacteria by keeping the concentration of antibiotics low enough to allow cells to synthesize resistance proteins encoded in plasmid DNA. In this case, it can product TetA protein and then separate more tetracycline from the cells. Ultimately, bacteria can become resistant under the influence of antibiotics.
This finding has broad relevance because AcrAB-TolC is highly conserved in bacteria and because its mechanism is not limited to tetracycline. Experiments have shown that the pump also allows bacteria to produce drug-resistant proteins in the presence of other antibiotics designed to inhibit gene expression, such as inhibition of translated chloramphenicol and rifampin, which inhibits transcription.
These results indicate that the bacterial AcrAB-TolC multidrug efflux pump can alleviate the blockade of tetracycline expression and at the same time establish antibiotic resistance.