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Summary: Hormonal steroids, such as progesterone, estrogen, testosterone, and ethinyl estradiol, can make gonorrhea resistant to antibiotics by allowing the bacterium to produce more efflux pumps, which help it resist antimicrobials. A study by Duke and Emory researchers found that a transcription factor called MtrR, which suppresses pump production, has an affinity for binding to these hormones, making it less effective. The bacterium can sense its hormonal environment and increases colonization during the week before ovulation when estrogen levels rise. This finding has implications for the treatment and prevention of gonorrhea.
You know that package warning that oral birth control won’t prevent STIs? Well in the case of gonorrhea, the sexually transmitted bacterium that causes the disease can use those hormones to help it resist antibiotic attacks.
Like many bacteria, this bug, Neisseria gonorrhoeae, is equipped with pumps to push the killing chemicals out of its cells. But what’s unique, according to a Duke and Emory study online this week in Nature Communications, is that the hormones of the human urogenital tract actually allow gonorrhea to make and use more of these pumps to fight intrinsic antimicrobials and prescribed antibiotics.
The researchers uncovered the trick while examining a transcription factor – a protein that binds to specific sites on the bacterium’s DNA and slows production of the efflux pumps that protect it.
Led by Duke graduate student Grace Hooks and her mentor, Biochemistry chair Richard Brennan, Ph.D., the study used a variety of approaches to characterize the shape and function of the transcription factor.
What they found is that, unfortunately, this transcription factor, called MtrR, has an affinity for binding to the hormonal steroids progesterone, estrogen and testosterone and the synthetic hormone ethinyl estradiol. When it binds to a hormone, the transcription factor becomes less effective at suppressing the production of bacterial pumps.
Hooks said the bacterium appears to be able to sense its hormonal environment and waits for the opportune time in the female’s menstrual cycle to ramp up its colonization.
Estrogen rises dramatically in the week before ovulation,