Repression of barrier gene expression, increased S. aureus-binding integrins in SLE keratinocytes found
WEDNESDAY, Feb. 12, 2020 (HealthDay News) — Patients with systemic lupus erythematosus (SLE) have increased colonization with Staphylococcus aureus in cutaneous lupus erythematosus lesions, according to a study recently published in the Journal of Investigative Dermatology.
Sirisha Sirobhushanam, Ph.D., from the University of Michigan in Ann Arbor, and colleagues examined the role of S. aureus, which is known to induce interferon (IFN) production, in cutaneous inflammation in patients with SLE. The impact of IFNs was examined on S. aureus colonization.
The researchers found that SLE patients were colonized at a higher rate than healthy adults (~40 versus ~30 percent), and active cutaneous lupus erythematosus lesions were highly colonized (~50 percent) by S. aureus. After exposure to both IFN-α and IFN-γ, there was an increase in adherent S. aureus, while IFN-γ seemed to inhibit S. aureus invasion. Repression of barrier gene expression, such as filaggrin and loricrin, was seen using data from cutaneous lupus erythematosus lesional skin microarray data and RNA sequencing data from SLE keratinocytes; increased S. aureus-binding integrins were seen in SLE keratinocytes. IFN treatment of keratinocytes replicated these SLE-associated changes. In addition, increased binding to S. aureus was seen for SLE keratinocytes.
“This is important because if true, the addition of topical antibiotics may be a simple way to improve treatment response in lupus skin and reduce the ability for those rashes to be colonized by staph,” a coauthor said in a statement.
Two authors disclosed financial ties to the pharmaceutical industry.
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