The Experts below are selected from a list of 837924 Experts worldwide ranked by ideXlab platform
Mayumi Komine - One of the best experts on this subject based on the ideXlab platform.
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Roxithromycin downregulates production of CTACK/CCL27 and MIP-3α/CCL20 from epidermal keratinocytes
Archives of dermatological research, 2010Co-Authors: Masaru Karakawa, Mayumi Komine, Kunihiko Tamaki, Mamitaro OhtsukiAbstract:Cutaneous T cell-attracting chemokine (CTACK)/CCL27 and macrophage inflammatory protein (MIP)-3α/CCL20 are the major inflammatory chemokines involved in skin inflammation. The present study showed that roxithromycin (RXM) suppressed the TNFα-induced production of CCL27 and CCL20 in HaCaT keratinocytes and normal human keratinocytes (NHKs) in a dose-dependent manner. The production of CCL20 induced by TNFα was suppressed by the addition of inhibitors of nuclear factor kappa B (NFκB). RXM suppressed NFκB activity induced by TNFα. RXM, by regulating CCL27 and CCL20, may contribute to the modulation of inflammation.
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roxithromycin downregulates production of ctack CCL27 and mip 3α ccl20 from epidermal keratinocytes
Archives of Dermatological Research, 2010Co-Authors: Mayumi Komine, Kunihiko Tamaki, Masaru Karakawa, Mamitaro OhtsukiAbstract:Cutaneous T cell-attracting chemokine (CTACK)/CCL27 and macrophage inflammatory protein (MIP)-3α/CCL20 are the major inflammatory chemokines involved in skin inflammation. The present study showed that roxithromycin (RXM) suppressed the TNFα-induced production of CCL27 and CCL20 in HaCaT keratinocytes and normal human keratinocytes (NHKs) in a dose-dependent manner. The production of CCL20 induced by TNFα was suppressed by the addition of inhibitors of nuclear factor kappa B (NFκB). RXM suppressed NFκB activity induced by TNFα. RXM, by regulating CCL27 and CCL20, may contribute to the modulation of inflammation.
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CCR4 and CCR10 are expressed on epidermal keratinocytes and are involved in cutaneous immune reaction.
Cytokine, 2008Co-Authors: Seiki Fujimoto, Hideya Uratsuji, Mayumi Komine, Yuichiro Tsunemi, Hidehisa Saeki, Shinji Kagami, Kunihiko TamakiAbstract:CC chemokine ligand (CCL)17 and CCL27 produced by epidermal keratinocytes (KCs) recruit CC chemokine receptor (CCR)4 and CCR10 expressing T cells into the skin, respectively, resulting in enhanced skin inflammation. However, CCR4/CCL17 and CCR10/CCL27 interactions in epidermal KCs have not been investigated. The purpose of this study was to evaluate the role of the CCR4/CCL17 and CCR10/CCL27 loops in cutaneous immune reaction. Normal human KCs (NHKs) and HaCaT KCs expressed both CCR4 and CCR10 at mRNA and protein levels. CCR4 ligand CCL17 but not CCR10 ligand CCL27 induced production of IL-12 p40, granulocyte/monocyte colony-stimulating factor (GM-CSF) and nerve growth factor (NGF) by KCs. Both CCL17 and CCL27 induced migration of KCs in Boyden chamber assay and wound scratch assay. This study revealed that CCR4 and CCR10 are expressed on epidermal KCs and that both are functional in terms of skin cytokine production and/or migration to their ligand CCL17 and CCL27, respectively. Thus this study provided new insight into chemokine/chemokine receptors of KCs.
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sezary syndrome treated with narrowband ultraviolet b time course measurement of serum levels of ccl17 CCL27
Clinical and Experimental Dermatology, 2007Co-Authors: Yuri Masui, Mayumi Komine, Hidehisa Saeki, Hideki Fujita, Makoto Sugaya, S. Kagami, Shoichiro Yano, M. Nagao, Hironobu Ihn, Kanako KikuchiAbstract:We describe a patient with Sezary syndrome (SS) who was successfully treated with topical steroid and narrowband UVB. Sezary cells in peripheral blood correlated with severity of skin lesions. In addition, serum levels of CCL17 and CCL27 decreased as disease activity improved. These chemokines may be important for the pathogenesis of SS.
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Sézary syndrome treated with narrowband ultraviolet B: time-course measurement of serum levels of CCL17/CCL27.
Clinical and experimental dermatology, 2006Co-Authors: Yuri Masui, Mayumi Komine, Hidehisa Saeki, Hideki Fujita, Makoto Sugaya, S. Kagami, Shoichiro Yano, M. Nagao, Hironobu Ihn, Kanako KikuchiAbstract:We describe a patient with Sezary syndrome (SS) who was successfully treated with topical steroid and narrowband UVB. Sezary cells in peripheral blood correlated with severity of skin lesions. In addition, serum levels of CCL17 and CCL27 decreased as disease activity improved. These chemokines may be important for the pathogenesis of SS.
Mamitaro Ohtsuki - One of the best experts on this subject based on the ideXlab platform.
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Roxithromycin downregulates production of CTACK/CCL27 and MIP-3α/CCL20 from epidermal keratinocytes
Archives of dermatological research, 2010Co-Authors: Masaru Karakawa, Mayumi Komine, Kunihiko Tamaki, Mamitaro OhtsukiAbstract:Cutaneous T cell-attracting chemokine (CTACK)/CCL27 and macrophage inflammatory protein (MIP)-3α/CCL20 are the major inflammatory chemokines involved in skin inflammation. The present study showed that roxithromycin (RXM) suppressed the TNFα-induced production of CCL27 and CCL20 in HaCaT keratinocytes and normal human keratinocytes (NHKs) in a dose-dependent manner. The production of CCL20 induced by TNFα was suppressed by the addition of inhibitors of nuclear factor kappa B (NFκB). RXM suppressed NFκB activity induced by TNFα. RXM, by regulating CCL27 and CCL20, may contribute to the modulation of inflammation.
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roxithromycin downregulates production of ctack CCL27 and mip 3α ccl20 from epidermal keratinocytes
Archives of Dermatological Research, 2010Co-Authors: Mayumi Komine, Kunihiko Tamaki, Masaru Karakawa, Mamitaro OhtsukiAbstract:Cutaneous T cell-attracting chemokine (CTACK)/CCL27 and macrophage inflammatory protein (MIP)-3α/CCL20 are the major inflammatory chemokines involved in skin inflammation. The present study showed that roxithromycin (RXM) suppressed the TNFα-induced production of CCL27 and CCL20 in HaCaT keratinocytes and normal human keratinocytes (NHKs) in a dose-dependent manner. The production of CCL20 induced by TNFα was suppressed by the addition of inhibitors of nuclear factor kappa B (NFκB). RXM suppressed NFκB activity induced by TNFα. RXM, by regulating CCL27 and CCL20, may contribute to the modulation of inflammation.
Masaru Karakawa - One of the best experts on this subject based on the ideXlab platform.
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Roxithromycin downregulates production of CTACK/CCL27 and MIP-3α/CCL20 from epidermal keratinocytes
Archives of dermatological research, 2010Co-Authors: Masaru Karakawa, Mayumi Komine, Kunihiko Tamaki, Mamitaro OhtsukiAbstract:Cutaneous T cell-attracting chemokine (CTACK)/CCL27 and macrophage inflammatory protein (MIP)-3α/CCL20 are the major inflammatory chemokines involved in skin inflammation. The present study showed that roxithromycin (RXM) suppressed the TNFα-induced production of CCL27 and CCL20 in HaCaT keratinocytes and normal human keratinocytes (NHKs) in a dose-dependent manner. The production of CCL20 induced by TNFα was suppressed by the addition of inhibitors of nuclear factor kappa B (NFκB). RXM suppressed NFκB activity induced by TNFα. RXM, by regulating CCL27 and CCL20, may contribute to the modulation of inflammation.
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roxithromycin downregulates production of ctack CCL27 and mip 3α ccl20 from epidermal keratinocytes
Archives of Dermatological Research, 2010Co-Authors: Mayumi Komine, Kunihiko Tamaki, Masaru Karakawa, Mamitaro OhtsukiAbstract:Cutaneous T cell-attracting chemokine (CTACK)/CCL27 and macrophage inflammatory protein (MIP)-3α/CCL20 are the major inflammatory chemokines involved in skin inflammation. The present study showed that roxithromycin (RXM) suppressed the TNFα-induced production of CCL27 and CCL20 in HaCaT keratinocytes and normal human keratinocytes (NHKs) in a dose-dependent manner. The production of CCL20 induced by TNFα was suppressed by the addition of inhibitors of nuclear factor kappa B (NFκB). RXM suppressed NFκB activity induced by TNFα. RXM, by regulating CCL27 and CCL20, may contribute to the modulation of inflammation.
Seon Il Jang - One of the best experts on this subject based on the ideXlab platform.
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Effect of persimmon leaf extract on utraviolet B-induced inflammation in HaCaT keratinocytes and mice
Journal of the Korean Society for Applied Biological Chemistry, 2011Co-Authors: Jung Keun Cho, Ji Min Park, In Hwa Jeon, Hyeon Soo Kim, Seon Il JangAbstract:Ultraviolet B (UVB) irradiation induces skin damage and inflammation. Persimmon leaf extract (PLE) has traditionally been used for the treatment of acute and chronic diseases in Asia, but there have been no reports on its UVB-protective effects. Thus, protective effects of PLE against UVB-induced inflammations in HaCaT keratinocytes and mice were investigated. In an in vitro study using HaCaT keratinocytes, UVB irradiation decreased cell viability and increased chemokine production. PLE recovered cell viability and suppressed UVB-induced production of monocyte chemotactic protein-1 (CCL2) and cutaneous T cell-attracting chemokine (CCL27). Moreover, oral administration of PLE to UVB-irradiated mice resulted in significant suppression of skin damage. Histological analyses revealed that infiltration of inflammatory cells, especially degranulated mast cells, thickening of the epidermis, and hyperplasia were significantly reduced. PLE treatment suppressed UVB-induced CCL2 and CCL27 expressions in the skin. These results suggest PLE has potential as an effective material for protection against UVB-induced skin inflammation.
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2s 2 methoxykurarinone from sophora flavescens suppresses cutaneous t cell attracting chemokine CCL27 expression induced by interleukin β tumor necrosis factor α via heme oxygenase 1 in human keratinocytes
Journal of Medicinal Food, 2010Co-Authors: Seung-il Jeong, Young-eun Lee, Seon Il JangAbstract:Abstract One of the CC chemokines, cutaneous T cell-attracting chemokine (CTACK/CCL27), is a skin-specific CC chemokine that is produced constitutively by keratinocytes and is highly up-regulated in inflammatory skin conditions such as atopic dermatitis and contact dermatitis. (2S)-2′-Methoxykurarinone (MOK) from Sophora flavescens has been demonstrated to have antioxidant effects. Heme oxygenase (HO)-1 has recently emerged as an important cytoprotective enzyme against oxidative stress and inflammatory responses in many cell types. This study aimed to define whether and how MOK regulates skin specific CTACK/CCL27 chemokine production in human HaCaT keratinocytes. The level of CTACK/CCL27 and HO-1 expression was measured by reverse transcription-polymerase chain reaction, and signaling was evaluated by western blot analysis. CTACK/CCL27 production was determined by enzyme-linked immunosorbent assay. Pretreatment with MOK suppressed tumor necrosis factor-α (TNF-α)- and interleukin (IL)-1β-induced CTACK/CCL2...
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Prenylated chalcone from Sophora flavescens suppresses Th2 chemokine expression induced by cytokines via heme oxygenase-1 in human keratinocytes.
Archives of pharmacal research, 2010Co-Authors: Byung-min Choi, Jang-won Lee, Ji Ye Mok, Dae Keun Kim, Seung-il Jeong, Seon Il JangAbstract:We recently reported the inhibitory effect of an oral administration of a Sophora flavescens Aiton methanol extract on the development of atopic dermatitis in the NC/Nga model mice. Heme oxygenase (HO)-1 has recently emerged as an important cytoprotective enzyme against oxidative stress and inflammatory responses in many cell types. The aim of this study was to investigate the possible mechanism by which prenylated chalcone (PC, 7,9,2′,4′-tetrahydroxy-8-isopentenyl-5-methoxychalcone), a natural product isolated from S. flavescens, inhibited cytokine-induced Th2 chemokine expression in human keratinocytes, HaCaT cells. The level of chemokine expression was measured by reverse transcription-polymerase chain reaction and HO-1 study was performed by Western blot analysis. Interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α)-induced thymus- and activation-regulated chemokine (TARC/CCL17), macrophage-derived chemokine (MDC/CCL22), cutaneous T-cell attracting chemokine (CTACK/CCL27) expression in a dose-dependent manner. Interestingly, PC significantly suppressed IFN-γ and TNF-α-induced TARC/CCL17, MDC/CCL22 and CTACK/CCL27 expression via the induction of heme oxygenase (HO)-1. This suppression was completely restored by HO-1 siRNA, suggesting a direct role of HO-1 for the suppressive effect. Furthermore, exogenous CO, but not other end products of HO-1 activity, also suppressed IFN-γ and TNF-α-induced TARC/CCL17, MDC/CCL22 and CTACK/CCL27 expression. These results demonstrate that prenylated chalcone induces HO-1 expression, which in turn HO-1 and/or CO suppresses Th2 chemokine expressions induced by cytokines in human HaCaT cells.
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(2S)-2′-Methoxykurarinone from Sophora flavescens Suppresses Cutaneous T Cell-Attracting Chemokine/CCL27 Expression Induced by Interleukin-β/Tumor Necrosis Factor-α via Heme Oxygenase-1 in Human Keratinocytes
Journal of medicinal food, 2010Co-Authors: Seung-il Jeong, Young-eun Lee, Seon Il JangAbstract:Abstract One of the CC chemokines, cutaneous T cell-attracting chemokine (CTACK/CCL27), is a skin-specific CC chemokine that is produced constitutively by keratinocytes and is highly up-regulated in inflammatory skin conditions such as atopic dermatitis and contact dermatitis. (2S)-2′-Methoxykurarinone (MOK) from Sophora flavescens has been demonstrated to have antioxidant effects. Heme oxygenase (HO)-1 has recently emerged as an important cytoprotective enzyme against oxidative stress and inflammatory responses in many cell types. This study aimed to define whether and how MOK regulates skin specific CTACK/CCL27 chemokine production in human HaCaT keratinocytes. The level of CTACK/CCL27 and HO-1 expression was measured by reverse transcription-polymerase chain reaction, and signaling was evaluated by western blot analysis. CTACK/CCL27 production was determined by enzyme-linked immunosorbent assay. Pretreatment with MOK suppressed tumor necrosis factor-α (TNF-α)- and interleukin (IL)-1β-induced CTACK/CCL2...
Kunihiko Tamaki - One of the best experts on this subject based on the ideXlab platform.
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Roxithromycin downregulates production of CTACK/CCL27 and MIP-3α/CCL20 from epidermal keratinocytes
Archives of dermatological research, 2010Co-Authors: Masaru Karakawa, Mayumi Komine, Kunihiko Tamaki, Mamitaro OhtsukiAbstract:Cutaneous T cell-attracting chemokine (CTACK)/CCL27 and macrophage inflammatory protein (MIP)-3α/CCL20 are the major inflammatory chemokines involved in skin inflammation. The present study showed that roxithromycin (RXM) suppressed the TNFα-induced production of CCL27 and CCL20 in HaCaT keratinocytes and normal human keratinocytes (NHKs) in a dose-dependent manner. The production of CCL20 induced by TNFα was suppressed by the addition of inhibitors of nuclear factor kappa B (NFκB). RXM suppressed NFκB activity induced by TNFα. RXM, by regulating CCL27 and CCL20, may contribute to the modulation of inflammation.
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roxithromycin downregulates production of ctack CCL27 and mip 3α ccl20 from epidermal keratinocytes
Archives of Dermatological Research, 2010Co-Authors: Mayumi Komine, Kunihiko Tamaki, Masaru Karakawa, Mamitaro OhtsukiAbstract:Cutaneous T cell-attracting chemokine (CTACK)/CCL27 and macrophage inflammatory protein (MIP)-3α/CCL20 are the major inflammatory chemokines involved in skin inflammation. The present study showed that roxithromycin (RXM) suppressed the TNFα-induced production of CCL27 and CCL20 in HaCaT keratinocytes and normal human keratinocytes (NHKs) in a dose-dependent manner. The production of CCL20 induced by TNFα was suppressed by the addition of inhibitors of nuclear factor kappa B (NFκB). RXM suppressed NFκB activity induced by TNFα. RXM, by regulating CCL27 and CCL20, may contribute to the modulation of inflammation.
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CCR4 and CCR10 are expressed on epidermal keratinocytes and are involved in cutaneous immune reaction.
Cytokine, 2008Co-Authors: Seiki Fujimoto, Hideya Uratsuji, Mayumi Komine, Yuichiro Tsunemi, Hidehisa Saeki, Shinji Kagami, Kunihiko TamakiAbstract:CC chemokine ligand (CCL)17 and CCL27 produced by epidermal keratinocytes (KCs) recruit CC chemokine receptor (CCR)4 and CCR10 expressing T cells into the skin, respectively, resulting in enhanced skin inflammation. However, CCR4/CCL17 and CCR10/CCL27 interactions in epidermal KCs have not been investigated. The purpose of this study was to evaluate the role of the CCR4/CCL17 and CCR10/CCL27 loops in cutaneous immune reaction. Normal human KCs (NHKs) and HaCaT KCs expressed both CCR4 and CCR10 at mRNA and protein levels. CCR4 ligand CCL17 but not CCR10 ligand CCL27 induced production of IL-12 p40, granulocyte/monocyte colony-stimulating factor (GM-CSF) and nerve growth factor (NGF) by KCs. Both CCL17 and CCL27 induced migration of KCs in Boyden chamber assay and wound scratch assay. This study revealed that CCR4 and CCR10 are expressed on epidermal KCs and that both are functional in terms of skin cytokine production and/or migration to their ligand CCL17 and CCL27, respectively. Thus this study provided new insight into chemokine/chemokine receptors of KCs.
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CCL28 production in HaCaT cells was mediated by different signal pathways from CCL27
Experimental dermatology, 2006Co-Authors: Shinji Kagami, Mayumi Komine, Yuichiro Tsunemi, Hidehisa Saeki, Takashi Kakinuma, Koichiro Nakamura, K. Sasaki, Akihiko Asahina, Kunihiko TamakiAbstract:Both CCL27 and CCL28 are ligands for CCR10 and attract CCR10(+) lymphocytes. We previously demonstrated that CCL27 and CCL28 were strongly expressed in sera and lesional keratinocytes of patients with atopic dermatitis and psoriasis vulgaris. However, the regulation of CCL27 and CCL28 production in keratinocytes has not been well documented. In this study, we showed that CCL27 and CCL28 expression and production by a human keratinocyte cell line, HaCaT cells, were strongly induced by inflammatory cytokines tumor necrosis factor-alpha and interleukin-1beta. CCL27 production was downregulated by inhibitors of p38 mitogen-activated protein kinase and nuclear factor-kappa B (NF-kappaB). By contrast, CCL28 production was downregulated by inhibitors of extracellular signal-regulated kinase and NF-kappaB. Our study results suggest that CCL28 produced by keratinocytes is mediated by different signal pathways from CCL27 and that both CCL27 and CCL28 are involved in the pathogenesis of inflammatory skin diseases.