NEW YORK (GenomeWeb) – Staphylococcus aureus becomes more abundant during flare-ups of eczema, according to a new study of the skin microbiome.
Skin bacteria are known to influence eczema, or atopic dermatitis. In this new study, researchers from the US National Institutes of Health performed metagenomic shotgun sequencing on samples obtained from atopic dermatitis patients before, during, and after a flare-up of their condition.
As they reported in Science Translational Medicine yesterday, the National Cancer Institute’s Heidi Kong and her colleagues found that S. aureus was more common among patients with more severe disease flares and that certain strains could elicit skin inflammation and immune response similar to eczema patients in a mouse model.
The researchers collected skin microbiome samples from 11 children with moderate to severe atopic dermatitis — disease severity was ascertained using the SCORAD assessment tool — and seven healthy children. The children were sampled at baseline, during a worsening of their condition, and after treatment, at seven different sites.
In all, the researchers performed shotgun metagenomic sequencing on 422 samples, and generated 191 gigabases of microbial sequence data that they mapped to a multi-kingdom reference database. Bacteria, they noted, dominated the samples.
Based on the Shannon diversity index, which measures both the total number of bacterial species and the proportion of species, the researchers noted that there was a reduction in diversity with increasing disease severity. Additionally, they found that severe disease was associated with a higher relative abundance of staphylococcal species.
In particular, patients with more severe disease flares had a higher relative abundance of S. aureus. By contrast, patients with less severe flares had a higher relative abundance of S. epidermidis. The team confirmed this association through cultures.
Kong and her colleagues said that this increase in S. aureus with disease severity could reflect either an overall increase in S. aureus strains or an increase in one strain in particular. With a strain tracking approach, they found that the more severe atopic dermatitis patients tended to be colonized by one S. aureus strain during a flare-up. That strain then persisted after the flare ended, but at a lower relative abundance. However, which strain predominated varied from patient to patient.
Though S. aureus has been associated with atopic dermatitis, the researchers noted that it wasn’t clear whether it was a cause of disease of a byproduct of it. By testing the effect of atopic dermatitis-associated S. aureus strains on mice, they found that certain S. aureus strains appeared to be enough to elicit the skin thickening and inflammatory response seen in atopic dermatitis patients.
The magnitude of the effect varied by strain, the researchers added. For instance, four S. aureus strains isolated from patients with severe disease led to the production in mice of the interleukin IL-13, which is associated with allergic response, as well as to the cutaneous infiltration of T helper 17 cells.
“[O]ur findings demonstrate that staphylococcal strains may play an important role in AD disease progression in a strain-specific manner,” the researchers wrote.