Seon-Pil Jin1, Zhenyu Li1, Eun Kyung Choi2, Serah Lee3, Yoen Kyung Kim3, Eun Young Seo3, Jin Ho Chung1, Soyun Cho4. 1. Department of Dermatology, Seoul National University College of Medicine, Republic of Korea; Institute of Human-Environmental Interface Biology, Medical Research Center, Seoul National University, Republic of Korea; Deparment of Biomedical Science, Seoul National University Graduate School, Republic of Korea. 2. Laboratory of Electron Microscope, Department of Pathology, Seoul National University Hospital, Seoul, Republic of Korea. 3. Department of Dermatology, Seoul National University College of Medicine, Republic of Korea; Institute of Human-Environmental Interface Biology, Medical Research Center, Seoul National University, Republic of Korea. 4. Department of Dermatology, Seoul National University College of Medicine, Republic of Korea; Institute of Human-Environmental Interface Biology, Medical Research Center, Seoul National University, Republic of Korea; Department of Dermatology, Seoul National University Boramae Medical Center, Republic of Korea. Electronic address: sycho@snu.ac.kr.
Abstract
BACKGROUND: Particulate matter (PM) is an integral part of air pollution, which is a mixture of particles suspended in the air. Recently, it has been reported that PM is associated with increased risks of skin diseases, especially atopic dermatitis in children. However, it is unclear if PM directly goes into the skin and what mechanisms are involved in response to PM. OBJECTIVE: To see whether PM could penetrate into the barrier-disrupted skin, produce reactive oxygen species (ROS), and elicit an inflammatory response. METHODS: We collected PMs during a winter in Seoul and used cultured keratinocytes for in vitro study and tape-stripped BALB/c mice for in vivo study. RESULTS: Keratinocyte cytotoxicity increased in a dose-dependent manner by PM treatment. IL-8 and MMP-1 mRNA expression and protein levels were significantly increased compared to control by qPCR and ELISA, respectively. Cellular ROS production was increased by PM treatment, and antioxidant N-acetyl cysteine pretreatment prevented induction of inflammatory cytokines IL-8 and MMP-1. In PM-treated keratinocytes, electron-dense subcellular particles were observed by transmission electron microscopy. PM was observed inside hair follicles in both intact and barrier-disrupted skin in vivo. Additionally, intercellular penetration of PM was seen in the barrier-disrupted skin. Repeated PM application induced epidermal thickening and dermal inflammation with neutrophil infiltration. Finally, N-acetyl cysteine could ameliorate skin inflammation induced by PM application. CONCLUSION: PM penetrates into the barrier-disrupted skin, causing inflammation, demonstrating detrimental effects in the skin.
BACKGROUND: Particulate matter (PM) is an integral part of air pollution, which is a mixture of particles suspended in the air. Recently, it has been reported that PM is associated with increased risks of skin diseases, especially atopic dermatitis in children. However, it is unclear if PM directly goes into the skin and what mechanisms are involved in response to PM. OBJECTIVE: To see whether PM could penetrate into the barrier-disrupted skin, produce reactive oxygen species (ROS), and elicit an inflammatory response. METHODS: We collected PMs during a winter in Seoul and used cultured keratinocytes for in vitro study and tape-stripped BALB/c mice for in vivo study. RESULTS: Keratinocyte cytotoxicity increased in a dose-dependent manner by PM treatment. IL-8 and MMP-1 mRNA expression and protein levels were significantly increased compared to control by qPCR and ELISA, respectively. Cellular ROS production was increased by PM treatment, and antioxidant N-acetyl cysteine pretreatment prevented induction of inflammatory cytokines IL-8 and MMP-1. In PM-treated keratinocytes, electron-dense subcellular particles were observed by transmission electron microscopy. PM was observed inside hair follicles in both intact and barrier-disrupted skin in vivo. Additionally, intercellular penetration of PM was seen in the barrier-disrupted skin. Repeated PM application induced epidermal thickening and dermal inflammation with neutrophil infiltration. Finally, N-acetyl cysteine could ameliorate skin inflammation induced by PM application. CONCLUSION: PM penetrates into the barrier-disrupted skin, causing inflammation, demonstrating detrimental effects in the skin.
Authors: Irini M Dijkhoff; Barbara Drasler; Bedia Begum Karakocak; Alke Petri-Fink; Giuseppe Valacchi; Marc Eeman; Barbara Rothen-Rutishauser Journal: Part Fibre Toxicol Date: 2020-07-25 Impact factor: 9.400