In people with eczema, S. aureus can evolve into a variant with a mutation in a specific gene that allows it to grow faster on the skin, according to a paper in Cell Host and Microbe.
The researchers, from MIT and other institutions, report this is the first time scientists have directly observed this rapid evolution in a microbe associated with a complex skin disorder, and could lead to the development of new therapies.
“This is the first study to show that Staph aureus genotypes are changing on people with atopic dermatitis,” said Tami Lieberman, an assistant professor of civil and environmental engineering and a member of MIT’s Institute for Medical Engineering and Science in a press release. “To my knowledge, this is the most direct evidence of adaptive evolution in the skin microbiome.”
In this study, the researchers explored how S. aureus adapts to living on the skin of eczema patients rather than in the nostrils where it normally resides. It is thought that the bacteria contribute to eczema because they secrete toxins and recruit immune cells, with this immune reaction further damaging the skin barrier.
The study group recruited 24 patients aged five to 15 years undergoing treatment for moderate to severe eczema. Samples of the microbes on their skin were taken once a month for three months, and again at nine months. The samples were obtained from the backs of the knees and inside of the elbows, the forearms, which are usually not affected by eczema, and the nostrils.
S. aureus cells from each sample site were cultured separately to create up to 10 colonies from each sample. The cell genome was sequenced when the colonies had grown sufficiently. A total of nearly 1,500 unique colonies were identified, which enabled the researchers to observe the bacterial cells’ evolution in much greater detail than previously possible.
Using this technique, the researchers found that most patients maintained a single lineage of S. aureus. However, within each lineage, significant mutation and evolution occurred during the nine months of the study.
“Despite the stability at the lineage level, we see a lot of dynamics at the whole genome level, where new mutations are constantly arising in these bacteria and then spreading throughout the entire body,” Lieberman said. She noted that many of these mutations took place in a gene known as capD, which encodes an enzyme necessary for synthesizing the capsular polysaccharide—the coating that protects S. aureus from recognition by immune cells. The capD mutations allowed S. aureus to grow faster than S. aureus strains with a normal capD, the researchers reported.
“Our findings in this study provide clues as to how Staph aureus is evolving inside hosts and reveal some of the features that might help the bacteria to stay on the skin and generate disease versus being able to be swiped off,” said Dr. Maria Teresa García-Romero, a co-author and dermatologist at the National Institute of Pediatrics in Mexico. “In the future, S. aureus variants with mutations in the capsular polysaccharide could be a relevant target for potential treatments.”
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