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WEDNESDAY, Feb. 12, 2020 (HealthDay News) — Patients with systemic lupus erythematosus (SLE) have increased colonization with Staphylococcus aureus<\/i> in cutaneous lupus erythematosus lesions, according to a study recently published in the Journal of Investigative Dermatology<\/i>.<\/p>\n
Sirisha Sirobhushanam, Ph.D., from the University of Michigan in Ann Arbor, and colleagues examined the role of S. aureus<\/i>, which is known to induce interferon (IFN) production, in cutaneous inflammation in patients with SLE. The impact of IFNs was examined on S. aureus<\/i> colonization.<\/p>\n
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<\/i>. After exposure to both IFN-\u03b1 and IFN-\u03b3, there was an increase in adherent S. aureus<\/i>, while IFN-\u03b3 seemed to inhibit S. aureus<\/i> 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<\/i>-binding integrins were seen in SLE keratinocytes. IFN treatment of keratinocytes replicated these SLE-associated changes. In addition, increased binding to S. aureus<\/i> was seen for SLE keratinocytes.<\/p>\n
“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.<\/p>\n
Two authors disclosed financial ties to the pharmaceutical industry.<\/p>\n
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