Staphylococcus aureus Colonization Is Increased on Lupus Skin Lesions and Is Promoted by IFN-Mediated Barrier Disruption.

ABSTRACT: Cutaneous inflammation is recurrent in systemic lupus erythematosus (SLE), yet mechanisms that drive cutaneous inflammation in SLE are not well defined. Type I IFNs are elevated in nonlesional SLE skin and promote inflammatory responses. Staphylococcus aureus, known to induce IFN production, could play a role in cutaneous inflammation in SLE. We show here that active cutaneous lupus erythematosus lesions are highly colonized (∼50%) by S. aureus. To define the impact of IFNs on S. aureus colonization, we examined the effects of type I and type II IFNs on S. aureus adherence and invasion. An increase in adherent S. aureus was observed after exposure to both IFN-α and -γ, whereas IFN-γ appeared to inhibit invasion of S. aureus. Cutaneous lupus erythematosus lesional skin microarray data and R

SUBMITTER: Sirobhushanam S 

PROVIDER: S-EPMC7183889 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature