One Pathogen’s Natural Enemy

New research from the University of Washington lends further insights into how nitric oxide—a chemical that is used as a preservative and is also naturally produced in the body—inhibits the growth of the Salmonella bacteria and may assist researchers looking for ways to combat the pathogen.

Ferric Fang, MD, a University of Washington professor of laboratory medicine and microbiology and an adjunct professor of medicine, is researching nitric oxide as part of his focus on how pathogenic bacteria like Salmonella cause disease—and how the bacteria attempt to resist the body’s efforts to kill them.

Dr. Fang’s new findings demonstrate that nitric oxide kills these pathogens by interfering with their energy production. “Nitric oxide imposes substantial metabolic restrictions on bacteria,” he said. It interacts with numerous metabolic targets, thwarting the growth of many disease-causing bacteria. Exposure to nitric oxide renders Salmonella incapable of making two key amino acids. Starved of these amino acids, methionine and lysine, Salmonella finds it difficult, if not impossible, to grow. Nitric oxide also blocks certain regulatory genes that Salmonella might use to try to find a way out of this roadblock. Fortunately for humans, we don’t need these same two amino acids for growth.

Salmonella is dependent on taking up these amino acids from the body,” said Dr. Fang. “This might be a key area of vulnerability for the pathogen. Understanding vulnerabilities like these in pathogenic bacteria is essential to devising strategies to inhibit these microbes from getting the things they’re trying to get. Only about 20 years ago was it discovered that nitric oxide is made by cells in the body and has a myriad of biological functions important to human health—it’s involved in neurotransmission, inhibition of cancer, and many other areas. We’re now learning much more about how it inhibits microbial growth as well.”

The latest research appears in the July 21 edition of Cell Host & Microbe. (Richardson AR, Payne EC, Younger N, et al. 2011;10(1):33-43.)


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