S aureus Nasal Colonization Associated With SLE Disease Phenotype

S aureus colonization was associated with particular SLE phenotypes.

Researchers have found that greater numbers of Staphylococcus aureus (SA) found in the nasal carriage seem to be associated with a specific systemic lupus erythematosus (SLE) phenotype that manifests in the skin and kidneys, and is characterized by autoantibody positivity.1 The findings were recently published in Arthritis Research & Therapy.

“In recent years there has been growing interest in the possible role of the microbiome in the development and course of disease. Of note, the gut microbiome has been widely investigated in autoimmune diseases, such as type 1 diabetes, inflammatory bowel diseases, rheumatoid arthritis, and spondyloarthropathies,”2 wrote Fabrizio Conti, MD, PhD, from the Lupus Clinic at Sapienza University of Rome and colleagues. “Conversely, few data are available on the skin microbiome and the relationship with autoimmune diseases.”

High Yield Data Summary

  • S aureus colonization was associated with particular SLE phenotypes, including renal & skin involvement and increased prevalence of autoantibodies

The researchers aimed to investigate the presence of the bacterium S aureus, a part of the human skin microbiome which causes pathogenic conditions ranging from minor infections to life-threatening diseases, in its most frequent location on the human body, the anterior nares.

Over a period of 3 months, 84 Caucasian participants with SLE who had been referred to the Lupus Clinic at Sapienza University of Rome were enrolled in the Sapienza Lupus Cohort, and 154 participants were enrolled as healthy controls. 

Their autoantibodies were analyzed, C3 and C4 serum levels evaluated, and both anterior nares were swabbed to evaluate the bacteria present in the nostrils. In the SLE cohort, disease activity was measured with the SLE Disease Activity Index 2000 (SLEDAI-2 k) and the European Consensus Lupus Activity Measurement (ECLAM).

The researchers found that there was not a significant difference between the prevalence of SA nasal colonization in participants with SLE vs healthy controls; the rate of SA nasal colonization was 21.4% in participants with SLE, and 28.6% in healthy controls.

However, in those with SA-positive SLE, renal involvement was significantly more frequent (11.6% vs 3.0%; P = .0009), and there was a significantly higher presence of anti-dsDNA, anti-Sm, anti-SSA, anti-SSB, anti-RNP antibodies in SA-positive SLE (P < .0001, P = .01, P = .008, P = .03, P = .03, respectively).

“Despite a similar frequency of SA being observed in patients and a healthy control group, the SA colonization in patients with SLE was associated with a specific disease phenotype, characterized by renal and skin involvement, and a higher prevalence of a broad spectrum of autoantibodies,” the authors wrote.

Summary & Clinical Applicability

Researchers examined SA colonization, a relatively frequent occurrence in SLE, and found that the presence of SA in the anterior nares seemed to be associated with a specific SLE phenotype characterized by manifestations on the skin and kidneys.  

While they were unable to determine whether this effect is causal or simply a secondary symptom, the authors noted that “the skin microbiome deserves deeper investigation, as it may influence disease onset and features.”

Limitations & Disclosures

  • SA colonization was identified with classical morphological evaluation, without molecular characterization
  • Cross-sectional study design evaluated nasal bacterial colonization at a single time point, which did not allow transient carriers to be excluded

The authors declare that they have no competing interests.


  1. Conti F, Ceccarelli F, Iaiani G, et al. Association between Staphylococcus aureus nasal carriage and disease phenotype in patients affected by systemic lupus erythematosus. Arthritis Res Ther. 2016;18:177. doi:10.1186/s13075-016-1079-x.
  2. McLean MH, Dieguez Jr D, Miller LM, Young HA. Does the microbiota play a role in the pathogenesis of autoimmune diseases? Gut. 2015;64:332–41.

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