Antibiotic-resistant strains of Staphlyococcus aureus bacteria (purple) have become the most common cause of skin infections seen in hospital emergency departments. Credit: NIH’s National Institute of Allergy and Infectious Diseases.
In the United States alone, at least 2 million people each year develop serious infections with bacteria that have become resistant to the antibiotics we use to combat them, and about 23,000 die, according to the Centers for Disease Control and Prevention. Antibiotic resistance can turn once-manageable infections into “superbug” diseases that are difficult—and sometimes impossible—to treat.
Scientists funded by the National Institutes of Health are studying many aspects of antibiotic resistance, including how it spreads. Read this Inside Life Science article for just a few research examples and how the work could aid efforts to curb the emergence of resistance.
Exposure to hypochlorous acid causes bacterial proteins to unfold and stick to one another, leading to cell death. Credit: Video segment courtesy of the American Chemistry Council. View video
Spring cleaning often involves chlorine bleach, which has been used as a disinfectant for hundreds of years. But our bodies have been using bleach’s active component, hypochlorous acid, to help clean house for millennia. As part of our natural response to infection, certain types of immune cells produce hypochlorous acid to help kill invading microbes, including bacteria.
Researchers funded by the National Institutes of Health have made strides in understanding exactly how bleach kills bacteria—and how bacteria’s own defenses can protect against the cellular stress caused by bleach. The insights gained may lead to the development of new drugs to breach these microbial defenses, helping our bodies fight disease.
Bacteroides ovatus. Credit: Eric Martens, University of Michigan Medical School.
After eating, we don’t do all the work of digestion on our own. Trillions of gut bacteria help us break food down into the simple building blocks our cells need to function. New research from an international team co-led by Eric Martens of the University of Michigan Medical School has uncovered how a strain of beneficial gut bacteria, Bacteroides ovatus, digests complex carbohydrates called xyloglucans that are found in fruits and vegetables. The researchers traced the microorganism’s digestive ability to a single piece of the genome. They also examined a publicly available set of genomic data, which included information from both humans and their resident bacteria, and found that more than 90 percent of 250 adults harbored at least one Bacteroides strain with xyloglucan-digesting capabilities. These results underscore the importance of the bacteria to human health and nutrition.
This work also was funded by the National Institute of Diabetes and Digestive and Kidney Diseases.
University of Michigan News Release
University of Michigan Host Microbiome Initiative
Gut Reactions and Other Findings About Our Resident Microbes from Inside Life Science
Body Bacteria from Findings Magazine
Productive V. cholerae (yellow) and exploitive V. cholerae (red). Credit: Carey Nadell, Princeton University.
What looks like an abstract oil painting is actually an image of several cholera-causing V. cholerae bacterial communities. These communities, called biofilms, include productive and exploitive microbial members. The industrious bacteria (yellow) tend to thrive in denser biofilms (top) while moochers (red) thrive in weaker biofilms (bottom). In an effort to understand this phenomenon, Princeton University researchers led by Bonnie Bassler discovered two ways the freeloaders are denied food. They found that some V. cholerae cover themselves with a thick coating to prevent nutritious carbon- and nitrogen-containing molecules from drifting over to the scroungers. In addition, the natural flow of fluids over biofilms can wash away any leftovers. Encouraging such bacterial fairness could boost the efficient breakdown of organic materials into useful products, such as biofuels. On the other hand, counteracting it could lead to better treatment of illnesses, like cholera, by starving the most productive bacteria and thereby weakening the infection.
Princeton University News Release
Like plants and animals, different types of E. coli thrive in different environments. Now, scientists can even predict which environments—such as the bladder, stomach or blood—are most amenable to the growth of various strains, including pathogenic ones. A research team led by Bernhard Palsson of the University of California, San Diego, accomplished this by using genome data to reconstruct the metabolic networks of 55 E. coli strains. The metabolic models, which identify differences in the ability to manufacture certain compounds and break down various nutrients, shed light on how certain E. coli strains become pathogenic and how to potentially control them. One approach could be depriving the deadly strains of the nutrients they need to survive in their niches. The researchers plan to use their new method to study other bacteria, such as those that cause staph infections.
This work also was funded by NIH’s National Cancer Institute.
University of California, San Diego News Release
Credit: Huey Huang, Rice University.
A new video, starring the toxin in bee venom, might help scientists design new drugs to combat bacterial infections. The video, by Rice University biophysicist Huey Huang , condenses 6.5 minutes into less than a minute to show how the toxin, called melittin, destroys an animal or bacterial cell.
What looks like a red balloon is an artificial cell filled with red dye. Melittin molecules are colored green and float on the cell’s surface like twigs on a pond. As melittin accumulates on the cell’s membrane, the membrane expands to accommodate it. In the video, the membrane stretches into a column on the left.
When melittin levels reach a critical threshold, countless pinhole leaks burst open in the membrane. The cell’s vital fluids—red dye in the video—leak out through these pores. Within minutes, the cell collapses.
Many organisms use such a pore-forming technique to kill attacking bacterial cells. This research reveals molecular-level details of the strategy, bringing pharmaceutical scientists a step closer to harnessing it in the design of new antibiotics.
Rice University News Release
A section of mouse colon with gut bacteria (center, in green) residing within a protective pocket. Credit: S. Melanie Lee, Caltech; Zbigniew Mikulski and Klaus Ley, La Jolla Institute for Allergy and Immunology.
Have you ever felt that your gut was trying to tell you something? The guts of germ-free mice have told scientists a few new things about our resident microorganisms. By studying a genus of bacteria called Bacteriodes that live in the gastrointestinal tract, Sarkis Mazmanian of the California Institute of Technology discovered how Bacteriodes species stake their claim in a mouse’s gut. Mazmanian and his colleagues introduced different species of Bacteriodes into germ-free mice to learn how the microbes competed and found that most of them peacefully co-existed. However, when microbes of a species that was already present were introduced, they couldn’t take up residence. Further investigation revealed that Bacteriodes species, due to a set of specific genes, can live in tiny pockets or “crypts” of the colon, where they are sheltered from antibiotics and infectious microbes passing through. Understanding how these microorganisms colonize could help devise ways to correct for abnormal changes in bacterial communities that are associated with disorders like inflammatory bowel disease.
This work also was funded by NIH’s National Institute of Diabetes and Digestive and Kidney Diseases.
California Institute of Technology News Release
Mazmanian Video Interview