Potential role of chemerin in recruitment of plasmacytoid dendritic cells to diseased skin.

Interferon alpha-producing plasmacytoid dendritic cells (pDC) are crucial contributors to pro-inflammatory or tolerogenic immune responses and are important in autoimmune diseases such as psoriasis. pDC accumulate in the lesional skin of psoriasis patients, but are rarely found in the affected skin of patients with atopic dermatitis (AD). While homeostatic chemokine CXCL12 and inducible pro-inflammatory CXCR3 chemokine ligands may regulate pDC influx to psoriatic skin, the mechanism responsible for selective pDC recruitment in psoriasis vs. AD remains unknown. Circulating pDC from normal donors express a limited number of chemoattractant receptors, including CXCR3 and CMKLR1 (chemokine-like receptor 1). In this work, we demonstrate that circulating pDC from normal donors as well as psoriasis and AD patients express similar levels of CXCR3 and responded similarly in functional migration assays to CXCL10. We next found that blood pDC from normal, AD, and psoriasis patients express functional CMKLR1. In contrast to normal skin, however, lesional skin from psoriasis patients contains the active form of the CMKLR1 ligand chemerin. Furthermore, in affected skin from psoriatic patients the level of active chemerin was generally higher than in AD skin. Taken together, these results indicate that local generation of active chemerin may contribute to pDC recruitment to psoriatic skin.

Susceptibility testing and resistance phenotype detection in Staphylococcus aureus strains isolated from patients with atopic dermatitis, with apparent and recurrent skin colonization.

BACKGROUND: Staphylococcus aureus colonization is accepted to be an important triggering factor in patients with atopic dermatitis (AD) and antibiotic resistance has been recognized to be a serious problem as a consequence and for the management of AD treatment. OBJECTIVES: To investigate the antibiotic resistance pattern of S. aureus strains isolated from patients with AD with apparent (lesional and nonlesional skin areas) and recurrent skin colonization and strains obtained from healthy nasal carriers. METHODS: Eighty-seven patients (age 23+/-11.5 years) with mild to severe AD (SCORAD 46.9+/-16.6), 21 patients (age 19.8+/-6.7 years) before antistaphylococcal treatment and 177 healthy nasal carriers (age 27.5+/-8.4 years) were microbiologically assessed for carriage of S. aureus. Colonization of lesional and nonlesional skin areas was quantified by counting the number of colony forming units on the skin surface (log(10) CFU cm(-2)). Antimicrobial susceptibility and resistance phenotypes of 179 S. aureus strains were assessed with the agar disc-diffusion method. RESULTS: Staphylococcus aureus was isolated from 87% of lesional and 44% of nonlesional skin samples from patients with AD. The colonization density of S. aureus was markedly higher in lesional than in nonlesional skin (P<0.001), and was positively correlated with AD severity (P<0.001) and total serum IgE (P<0.05). Patients with AD had a significantly higher prevalence of chloramphenicol-resistant S. aureus than nasal carriers (P<0.01). Similar rates of resistance were expressed to tetracycline, erythromycin, mupirocin, clindamycin and penicillin. Nearly 35% of S. aureus strains from the lesional skin demonstrated different antimicrobial sensitivity pattern compared with strains from nonlesional skin of the same patients with AD. The trend of increasing resistance to chloramphenicol, erythromycin and fusidic acid was observed among S. aureus strains recovered from patients after approximately 75 days of antibiotic treatment. Methicillin-resistant S. aureus isolates were cultured from two patients, one during exacerbation and the other after subsequent bacterial recolonization. CONCLUSIONS: Discrepancies in antibiotic sensitivity pattern were observed among S. aureus strains colonizing different sites of AD skin (lesional and nonlesional areas), and also in AD patients with prior antibiotic treatment. Therefore, clinicians should consider repeat microbial susceptibility testing on different body sites of patients with AD when clinically indicated.