A common breast cancer medication helps the body's immune system destroy an increasingly drug-resistant strain of bacteria that has plagued patients for years.
Bacteria are a serious concern for anyone, but especially for patients receiving treatment for life-threatening diseases like cancer. Public health officials have sounded the alarm about drug-resistant bacteria in hospitals across the country, and infections are on the rise.
There may be a new weapon in the fight against resistant bacteria, however. According to a press release from Eurekalert, researchers from the University of California, San Diego School of Medicine and Skaggs School of Pharmacy and Pharmaceutical Sciences have discovered that a medication used to treat breast cancer patients, tamoxifen, helps bolster the body’s immune system to kill off ‘superbacteria’ that have developed resistance to normal antibiotics.
The researchers also found that tamoxifen helped mice kill off the bacteria that causes MRSA, reducing overall mortality. The study’s findings were published today in the journal Nature Communications.
According to lead author Victor Nizet, a professor of pediatrics and pharmacy, bacteria that are resistant to multiple drugs present a growing threat. What’s even worse is that pharmaceutical companies are struggling to keep up with the demand for effective new antibiotics. The study aimed to find an existing safe medication that could also be used to fend off the advance of drug-resistant bacteria.
Tamoxifen works by targeting the body’s estrogen receptor. This makes the drug particularly useful for identifying cancer cells that show the hormone in great numbers. The researchers found that tamoxifen also has other properties that can be useful in fighting off disease.
The drug also influences the cells’ production of fatty molecules, or sphingolipids, separately from the estrogen receptors. These molecules are essential in regulating white blood cells, which serve as the body’s primary defense against invading pathogens.
The doctors theorized that this effect could help promote the destruction of bacteria that were immune to antibiotics. To test the hypothesis, they incubated a molecule produced by white blood cells, called neutrophilis, with a dose of tamoxifen. They compared the sample to an untreated sample of neutrophilis, and found that the treated sample had engulfed a higher percentage of bacteria.
The treated sample also created three times more neutrophil extracellular traps, a combination of DNA, antibacterial peptides, and enzymes that reach out and destroy germs.
The medication had little effect on healthy estrogen receptors, suggesting that the two effects of the drug are independent of each other. They tested the immune properties of the drug on mice, and found that the drug significantly protected them from infection. Mice treated with tamoxifen were five times more likely to become infected with MRSA bacteria than the untreated mice.
While the drug was effective at killing off MRSA, researchers are still unsure how it will fare against other bacteria. They also fear that too many neutrophil extracellular traps in the body could be harmful, creating internal inflammation.
The researchers will continue studying the antibacterial properties of tamoxifen, and perhaps even discover new drugs that could help prevent infections.