We investigated sodium lauryl sulfate (SLS)-skin reactions because of its relevance in patch tests of patients, and we compared its effects with ACD-inducing oxazolone (OXA) and ICD-inducing croton oil (CrO). SLS-induced contact dermatitis differed from classical ACD and ICD, as it elicited less pronounced immune alterations.
Abstract
Sodium lauryl sulfate (SLS) is used as a control irritant in patch testing for allergic contact dermatitis (ACD). However, up to 20% of those tested react to SLS, whereby the pathophysiological basis of this reaction is still unclear. To mimic patch test reactions, we repeatedly applied SLS to the skin of wild-type mice. Reactions were compared with those in a classical ACD model induced by oxazolone and an irritant contact dermatitis (ICD) model induced by croton oil. Skin inflammation was assessed with ear thickness measurements, immunohistochemistry, qRT-PCR, and flow cytometry. Topical SLS treatment was further investigated in Flg/Hrnr
−/−, Myd88/Tlr3
−/−, and Rag1
−/− mouse models. All three compounds caused ear swelling with different courses. Oxazolone treatment, compared with the ICD model, resulted in a greater influx of immune cells (CD4+, MHCII+, CD11b+). Similarly, SLS did not induce immune cell infiltration or expression of selected inflammatory and regulatory cytokines. SLS induced the most pronounced keratinocyte proliferation. Compared with wild-type mice, topical SLS application did not increase ear swelling in skin barrier deficient Flg/Hrnr
−/− mice, but led to significantly delayed swelling in mice with defects in innate or adaptive immune functions (Myd88/Tlr3
−/−, Rag1
−/−). SLS-induced contact dermatitis differed from classical ACD and ICD, as it elicited less pronounced immune alterations. Skin barrier impairment does not affect SLS-induced contact dermatitis, whereas both innate and adaptive components are involved in SLS skin reactions.