Background/Aims: There is increasing evidence that exposure to air pollutants, including particulate matter (PM_2.5, PM₁₀), nitrogen dioxide (NO₂), and sulfur dioxide (SO₂), might aggravate preexisting skin diseases such as eczema and urticaria. Here we investigated if a possible link exists between air pollution and acne vulgaris. We assessed the association between ambient air pollutant concentrations and the number of visits of patients for acne vulgaris to a dermatological outpatient clinic in Beijing, China, from April 1, 2012 to April 30, 2014. Methods: In this time period, 59,325 outpatient visits were recorded because of acne vulgaris. Daily air pollution parameters for PM₁₀, PM_2.5, SO₂, and NO₂ were obtained from the Beijing Municipal Environmental Monitoring Center. Results: Increased concentrations of ambient PM_2.5, PM₁₀, and NO₂ were significantly associated with increased numbers of outpatient visits for acne vulgaris over the 2 years. These effects could be observed for NO₂ in a single-pollutant model and for PM_2.5, PM₁₀, and NO₂ in 2-pollutant models, which are closer to real-life exposure. Of note, these effects were specific because they were not observed for increased SO₂ concentrations, which even showed negative correlations in all test models. Conclusion: This study provides indirect evidence for a link between acne vulgaris and air pollution.

No abstract

No abstract

No abstract

Interleukin (IL)-33 is a novel member of the IL-1 superfamily of cytokines that has recently become a focal point for research into the pathogenesis of atopic dermatitis (AD). However, the expression and regulation of IL-33 in human epidermal keratinocytes have not well been delineated. The aim of this study was to evaluate IL-33 and its receptor ST2L expression in skin lesions of AD patients and explored the signal transduction mechanisms leading to the IL-33 expression and of the IL-33's pharmacological action in keratinocytes from AD patients (ADKs) and those from healthy controls (NHEKs). We performed immunocytochemistry, reverse transcription-polymerase chain reaction, Western blotting, and enzyme-linked immunosorbent assay to investigate ADKs compared with NHEKs. We found that IL-33/ST2L were positively expressed in the skin lesions of AD patients and a high expression of IL-33 was induced in keratinocytes by IL-4 plus interferon [IFN]-γ or IFN-γ alone at the mRNA and protein levels. Meanwhile, IFN-γ induced IL-33 expression through extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase (MAPK), epidermal growth factor receptor (EGFR), and Janus kinase/signal transducer and activator of transcription. The expression of ST2L was increased in a time- and dose-dependent manner in both types of cells incubated with IL-33, and was especially increased in ADKs compared with NHEKs. We examined the cytokine IL-6 and the chemokines CXCL-8/IL-8, CCL-20, CCL-17, CCL-5, and CCL-2 in keratinocytes, which showed increased expression in a time- and dose-dependent manner in ADKs when induced by IL-33. Furthermore, 4 signaling pathways (ERK, p38 MAPK, c-Jun N-terminal kinase, and nuclear factor-κB) were involved in the IL-33-mediated induction in both cells. In conclusion, IL-33 is closely interlinked in AD skins and keratinocytes. IL-33 plays an important role in the pathogenesis of immune inflammatory responses in AD, which might be a possible therapeutic target in the treatment of AD.