Woon-Hae Kim1, Hyun-Jin An2, Jung-Yeon Kim3, Mi-Gyeong Gwon4, Hyemin Gu5, Sun-Jae Lee6, Ji Y Park7, Kyung-Duck Park8, Sang-Mi Han9, Min-Kyung Kim10, Kwan-Kyu Park11. 1. Department of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address: kimwoonhae@cu.ac.kr. 2. Department of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address: ahj119@cu.ac.kr. 3. Department of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address: jy1118@cu.ac.kr. 4. Department of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address: daldy99@naver.com. 5. Department of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address: asdf8760@naver.com. 6. Department of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address: pathosjlee@cu.ac.kr. 7. Department of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address: pathpjy@naver.com. 8. Department of Dermatology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address: gdpk1217@naver.com. 9. Department of Agricultural Biology, National Academy of Agricultural Science, Rural Development Administration, 300, Nongsaengmyeong-ro, Wansan-gu, Jeonju-si, Jeollabuk-do 54875, Republic of Korea. Electronic address: sangmih@korea.kr. 10. Department of Pathology, College of Medicine, Dongguk University, 123, Dongdae-ro, Gyeongju-si, Gyeongsangbuk-do 38066, Republic of Korea. Electronic address: minkyungk76@naver.com. 11. Department of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address: kkpark@cu.ac.kr.
Abstract
BACKGROUND: Atopic dermatitis (AD) is identified by an increase in infiltrations of several inflammatory cells including type 2 helper (Th2) lymphocytes. Th2-related chemokines such as thymus and activation-regulated chemokine (TARC/CCL17) and macrophage-derived chemokine (MDC/CCL22), and pro-inflammatory cytokines including interleukin (IL)-1β and IL-6 are considered to play a crucial role in AD. Tumor necrosis factor (TNF)-α- and interferon (IFN)-γ induce the inflammatory condition through production of TARC, MDC, IL-1β and IL-6, and activations of related transcription factors, such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and signal transducer and activator of transcription (STAT) in keratinocytes. Apamin, a peptide component of bee venom, has been reported its beneficial activities in various diseases. However, anti-inflammatory effects of apamin on inflammatory condition in keratinocytes have not been explored. Therefore, the present study aimed to demonstrate the anti-inflammatory effect of apamin on TNF-α- and IFN-γ-induced inflammatory condition in keratinocytes. METHODS: HaCaT was used as human keratinocytes cell line. Cell Counting Kit-8 was performed to measure a cytotoxicity of apamin. The effects of apamin on TNF-α-/IFN-γ-induced inflammatory condition were determined by real-time PCR and Western blot analysis. Further, NF-κB signaling pathways, STAT1, and STAT3 were analyzed by Western blot and immunofluorescence. RESULTS: Apamin ameliorated the inflammatory condition through suppression of Th2-related chemokines and pro-inflammatory cytokines. Further, apamin down-regulated the activations of NF-κB signaling pathways and STATs in HaCaT cells. CONCLUSIONS: These results suggest that apamin has therapeutic effect on AD through improvement of inflammatory condition.
BACKGROUND:Atopic dermatitis (AD) is identified by an increase in infiltrations of several inflammatory cells including type 2 helper (Th2) lymphocytes. Th2-related chemokines such as thymus and activation-regulated chemokine (TARC/CCL17) and macrophage-derived chemokine (MDC/CCL22), and pro-inflammatory cytokines including interleukin (IL)-1β and IL-6 are considered to play a crucial role in AD. Tumor necrosis factor (TNF)-α- and interferon (IFN)-γ induce the inflammatory condition through production of TARC, MDC, IL-1β and IL-6, and activations of related transcription factors, such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and signal transducer and activator of transcription (STAT) in keratinocytes. Apamin, a peptide component of bee venom, has been reported its beneficial activities in various diseases. However, anti-inflammatory effects of apamin on inflammatory condition in keratinocytes have not been explored. Therefore, the present study aimed to demonstrate the anti-inflammatory effect of apamin on TNF-α- and IFN-γ-induced inflammatory condition in keratinocytes. METHODS: HaCaT was used as human keratinocytes cell line. Cell Counting Kit-8 was performed to measure a cytotoxicity of apamin. The effects of apamin on TNF-α-/IFN-γ-induced inflammatory condition were determined by real-time PCR and Western blot analysis. Further, NF-κB signaling pathways, STAT1, and STAT3 were analyzed by Western blot and immunofluorescence. RESULTS: Apamin ameliorated the inflammatory condition through suppression of Th2-related chemokines and pro-inflammatory cytokines. Further, apamin down-regulated the activations of NF-κB signaling pathways and STATs in HaCaT cells. CONCLUSIONS: These results suggest that apamin has therapeutic effect on AD through improvement of inflammatory condition.
Authors: Léa C Castellucci; Lucas Almeida; Svetlana Cherlin; Michaela Fakiola; Richard W Francis; Edgar M Carvalho; Anadílton Santos da Hora; Tainã Souza do Lago; Amanda B Figueiredo; Clara M Cavalcanti; Natalia S Alves; Katia L P Morais; Andréa Teixeira-Carvalho; Walderez O Dutra; Kenneth J Gollob; Heather J Cordell; Jenefer M Blackwell Journal: Clin Infect Dis Date: 2021-05-18 Impact factor: 9.079