Using a combination of sequencing techniques, researchers from NIAMS and the National Human Genome Research Institute (NHGRI) surveyed the skin microbiome of patients with atopic dermatitis (AD, also called eczema) to understand the genetic diversity of the bacteria present on the skin and how genetic variants may contribute to disease severity. The study identified specific staphylococcal strains and genes associated with disease presence and severity. Other factors, such as regional differences in antibiotic use, within-household transmission of bacteria, and the transfer of genes among bacterial cells influenced the genetic diversity of the bacterial strains found on the skin of patients with AD.
This study, which appeared in the journal Cell Host and Microbe on April 12, 2023, provides a wealth of information about the vast diversity of skin microbes in AD. This could inform efforts to identify potential new therapeutics for preventing or treating severe disease.
AD is an inflammatory skin disease that causes redness, irritation, scaly rashes, and extreme itching. The likelihood of developing AD is greater if there is a family history of AD, allergies, or asthma, indicating that human genetics plays a part. External or environmental factors, such as dry air, excessive sweating, and the use of certain soaps or fragrances also influence the development of AD in those who are genetically susceptible.
People with AD disease flares also tend to have increased Staphylococcus species such as Staphylococcus aureus (S. aureus) and Staphylococcus epidermidis (S. epidermidis) on their skin. Previous studies in mice have suggested that S. aureus may make AD lesions worse and may affect how the immune system functions at the skin site. However, tremendous genomic variability exists even within the same staphylococcal species, and researchers do not fully know which genetic components may be associated with AD or how genetic differences may shape disease severity.
To understand the genomic variability of staphylococcal strains present on the skin of patients with AD, researchers sequenced skin swabs from patients with moderate-to-severe AD and from people with no history of AD. The two sequencing techniques used allowed the researchers to identify and study the genomes of all the bacterial species present on the skin. The research team also looked at all publicly available sequencing data from AD skin swabs from around the world to identify staphylococcal genes associated with AD.
The researchers also found that among one family living together in the same household, members had some of the same bacterial strains on their skin, suggesting that strains can be transmitted, or spread, among family members.
“Antibiotic treatments and strain-sharing within households can shape what we see colonizing the skin,” said the study’s senior author Heidi H. Kong, M.D., M.H.Sc., who is head of the NIAMS Intramural Research Program’s Cutaneous Microbiome and Inflammation Section.
Specific causal relationships were not examined as part of the study, but the researchers discovered that some staphylococcal strains were more commonly found on the skin of patients with AD than on patients with no history of AD. Further, S. aureus and S. epidermidis found on the skin of patients with severe disease were more likely to harbor genes involved in binding to the skin and in using energy (e.g., metabolism), respectively. In addition, an investigation of the genomes of different bacterial species showed evidence for the transfer of genetic components across species.
“This study showed that the genomic content of staphylococcal species found on the skin of atopic dermatitis patients is even more heterogeneous than we originally thought,” said Kong. Future studies will further examine this diversity to validate which bacterial strains worsen AD, and which do not.
Staphylococcal diversity in atopic dermatitis from an individual to a global scale.
Saheb Kashaf S, Harkins CP, Deming C, Joglekar P, Conlan S, Holmes CJ; NISC Comparative Sequencing Program; Almeida A, Finn RD, Segre JA, Kong HH.
Cell Host Microbe. 2023 Apr 12;31(4):578-592.e6. doi: 10.1016/j.chom.2023.03.010.