Staphylococcus aureus drives type I interferon-mediated monocyte recruitment and skin barrier disruption in cutaneous lupus erythematosus lesions
Presentation Time: 03:15 PM - 04:30 PM
Poster Board Number: B524
Abstract ID: 5574
Presenting Author:
Lisa Abernathy-Close , Research Investigator at Michigan Med., Univ. of Michigan
Abstract:
Cutaneous lupus erythematosus (CLE) is an inflammatory skin manifestation of systemic lupus erythematosus (SLE). While type I interferons (IFNs) are known to promote inflammation in SLE skin, the precise mechanisms driving SLE-associated cutaneous inflammation remain poorly defined. We previously demonstrated that CLE lesions are highly colonized with Staphylococcus aureus (S. aureus), a microbe known to promote IFN production. Here, we follow up to investigate whether type I IFN and inflammatory gene signatures in CLE lesions can be modulated with topical mupirocin, an antibiotic treatment against S. aureus skin infection. SLE patients with skin involvement were recruited from the Michigan Lupus Cohort (n = 12). Patients were randomized into treatment with either mupirocin or vehicle control, and lesional skin swabs and biopsies were collected before and after 7 days of treatment. Baseline and post-treatment Staphylococcus abundance was determined by 16S rRNA gene sequencing and inflammatory responses were evaluated by RNA-seq. Mupirocin treatment decreased the abundance of Staphylococcus associated with CLE lesions without altering the diversity of the skin microbiota relative to vehicle, and this correlated with decreased IFN pathway signaling and inflammatory gene expression in lesional skin. This study suggests that a topical antibiotic could be employed decrease lupus skin inflammation and cutaneous type I IFN responses by reducing Staphylococcus colonization.
Staphylococcus aureus drives type I interferon-mediated monocyte recruitment and skin barrier disruption in cutaneous lupus erythematosus lesions
Category
Poster