In patients with systemic lupus erythematosus (SLE) about half of active cutaneous lupus erythematosus lesions are highly colonised by S. aureus, a US study has found.

The infiltration of S. aureus appears to be mediated by chronic exposure to interferons in the auto-inflammatory condition,  which cause barrier disruption and increase the adherence of the staph.

Researchers at the University of Michigan made the discovery when they followed up earlier findings of interferon effects on skin sensitivity to sunlight and inflammation in lupus,

In a study of 51 patients with SLE they found that around 40% overall were colonised by S. aureus in areas including the nose and chest, a higher rate than that reported in healthy adults (∼30%). The rate of s. aureus colonisation was around 50% when active skin lesions were sampled.

The researchers said the rates of colonisation in SLE lesions were much higher than in a control group of patients with psoriasis, of whom none had staph detected in samples from lesions.

This was likely related to interferon IFN levels, they hypothesised, since people with SLE have high levels of IFN-1 where people with psoriasis have a mixed T helper type 1/T helper type 17 signature and low IFN levels.

They also found that the presence of S. aureus on the SLE rash was associated with higher cutaneous disease activity.

In subsequent experiments using microarray analysis of SLE lesional skin they found that IFN-stimulated genes and IFNs including IFN-κ, a regulator in keratinocytes for type I responses, were elevated significantly in cutaneous lupus lesions while genes responsible for barrier function were downregulated. And an increase in adherent S. aureus was observed after exposure to IFNs.

“This suggests that the high IFN environment may downregulate the epidermal barrier, which could promote S. aureus colonisation,” the authors wrote in the Journal of Investigative Dermatology.

Study investigator Dr Michelle Kahlenberg said the group focused on Staph aureus because it is a leading cause of infection in patients with lupus.

“Others have shown it may be associated with disease flares and development of lupus nephritis, or inflammation of the kidney in patients with lupus,” she said.

Dr Kahlenberg said she is now enrolling patients in a clinical trial that is testing whether topical antibiotics can decrease inflammation and rashes in the skin of patients with lupus.

“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 colonised by staph,” she said.