scholarly journals Anti-Allergic and Anti-Inflammatory Effects of Kuwanon G and Morusin on MC/9 Mast Cells and HaCaT Keratinocytes

Molecules ◽  
2019 ◽  
Vol 24 (2) ◽  
pp. 265 ◽  
Author(s):  
Seong Jin ◽  
Hyekyung Ha ◽  
Hyeun-Kyoo Shin ◽  
Chang-Seob Seo
Keyword(s):  
Mast Cells ◽  
Western Blotting ◽  
Skin Diseases ◽  
Hacat Keratinocytes ◽  
Inflammatory Skin Diseases ◽  
Histamine Production ◽  
Tnf Α ◽  
Ifn Γ ◽  
Inflammatory Skin ◽  
Anti Inflammatory

Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disease. The use of immunomodulatory corticosteroids in AD treatment causes adverse side effects. Therefore, novel natural anti-inflammatory therapeutics are needed. The aim of the present study was to investigate the anti-allergic and anti-inflammatory activities of kuwanon G and morusin. To investigate the effect of kuwanon G and morusin on skin inflammation, enzyme-linked immunosorbent assays (ELISA) to quantitate secreted (RANTES/CCL5), thymus- and activation-regulated chemokine (TARC/CCL17), and macrophage-derived chemokine (MDC/CCL22) were performed, followed by Western blotting to measure the phosphorylation of signal transducer and activator of transcription 1 (STAT1) and nuclear transcription factor-κB (NF-κB) p65 in tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ)-stimulated HaCaT keratinocytes. In order to evaluate the anti-allergic effects, ELISA to quantify histamine and leukotriene C4 (LTC4) production and Western blotting to measure 5-lipoxygenase (5-LO) activation were performed using PMA and A23187-stimulated MC/9 mast cells. Kuwanon G reduced the release of RANTES/CCL5, TARC/CCL17, and MDC/CCL22 via down-regulation of STAT1 and NF-κB p65 signaling in TNF-α and IFN-γ-stimulated HaCaT keratinocytes. Kuwanon G also inhibited histamine production and 5-LO activation in PMA and A23187-stimulated MC/9 mast cells. Morusin inhibited RANTES/CCL5 and TARC/CCL17 secretion via the suppression of STAT1 and NF-κB p65 phosphorylation in TNF-α and IFN-γ-stimulated HaCaT keratinocytes, and the release of histamine and LTC4 by suppressing 5-LO activation in PMA and A23187-stimulated MC/9 mast cells. Kuwanon G and morusin are potential anti-inflammatory mediators for the treatment of allergic and inflammatory skin diseases such as AD.

scholarly journals Water Extract of Rubus coreanus Prevents Inflammatory Skin Diseases In Vitro Models

Plants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1230
Author(s):  
Sumin Pyeon ◽  
Ok-Kyung Kim ◽  
Ho-Geun Yoon ◽  
Shintae Kim ◽  
Kyung-Chul Choi ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Skin Diseases ◽  
Water Extract ◽  
Total Phenolic ◽  
Hacat Cells ◽  
Rubus Coreanus ◽  
Tnf Α ◽  
Ifn Γ ◽  
Inflammatory Skin

Atopic dermatitis (AD) is a chronic inflammatory skin disease caused by immune hypersensitivity reaction. The cause of AD is unclear, but its symptoms have a negative effect on quality of life; various treatment methods to alleviate these symptoms are underway. In the present study, we aimed to evaluate in vitro antioxidant and anti-inflammatory effects of Rubus coreanus water extract (RCW) on AD. Total phenolic compounds and flavonoid content of RCW were 4242.40 ± 54.84 mg GAE/g RCE and 1010.99 ± 14.75 mg CE/g RCW, respectively. RCW reduced intracellular reactive oxygen species level and increased the action of antioxidant enzymes, such as catalase, superoxide dismutase, and glutathione peroxidase in tumor necrosis factor-α (TNF-α)/interferon-γ (IFN-γ)-stimulated HaCaT cells. Moreover, mRNA expression of the pro-inflammatory cytokines, including TNF-α, interleukin-1β, and interleukin-6, was downregulated by RCW in the TNF-α/IFN-γ-stimulated cells. The levels of inflammatory chemokines (thymus- and activation-regulated chemokine; eotaxin; macrophage-derived chemokine; regulated on activation, normal T-cell expressed and secreted; and granulocyte-macrophage colony-stimulating factor) and intercellular adhesion molecule-1 were decreased in the TNF-α/IFN-γ-stimulated HaCaT cells after RCW treatment. Additionally, the mRNA expression levels of filaggrin and involucrin, proteins that form the skin, were increased by RCW. Furthermore, RCW inhibited the nuclear factor kappa-light-chain-enhancer of the activated B cells pathway in the TNF-α/IFN-γ-stimulated HaCaT cells. Collectively, the present investigation indicates that RCW is a potent substance that inhibits AD.

scholarly journals Immunomodulatory properties of umbilical cord blood-derived small extracellular vesicles and their therapeutic potential for inflammatory skin disorders

2021 ◽  
Author(s):  
Silvia C Rodrigues ◽  
Renato M S Cardoso ◽  
Patricia C Freire ◽  
Claudia F Gomes ◽  
Filipe V Duarte ◽  
...  
Keyword(s):  
Cord Blood ◽  
Umbilical Cord ◽  
Extracellular Vesicles ◽  
Umbilical Cord Blood ◽  
Skin Diseases ◽  
Therapeutic Potential ◽  
Psoriatic Skin ◽  
Inflammatory Skin Diseases ◽  
Inflammatory Skin ◽  
Anti Inflammatory

Umbilical cord blood (UCB) has long been seen as a rich source of naive cells with strong regenerative potential, likely mediated by small extracellular vesicles (sEV). More recently, small extracellular vesicles (sEV), such as exosomes, have been shown to play essential roles in cell-to-cell communication, via the transport of numerous molecules, including small RNAs. Often explored for their potential as biomarkers, sEV are now known to have regenerative and immunomodulating characteristics, particularly if isolated from stem cell-rich tissues. In this study, we aim to characterize the immunomodulating properties of umbilical cord blood mononuclear cell sEV (herein referred as Exo-101), and explore their therapeutic potential for inflammatory skin diseases. Exo-101 was shown to shift macrophages toward an anti-inflammatory phenotype, which in turn exert paracrine effects on fibroblasts, despite previous inflammatory stimuli. Additionally, the incubation of PBMC with Exo-101 resulted in an reduction of total CD4+ and CD8+ T-cell proliferation and cytokine release, while specifically supporting the development of regulatory T-cells (Treg), by influencing FOXP3 expression. In a 3D model of psoriatic skin, Exo-101 reduced the expression of inflammatory and psoriatic markers IL-6, IL-8, CXCL10, COX-2, S100A7 and DEFB4. In vivo, Exo-101 significantly prevented or reversed acanthosis in imiquimod-induced psoriasis, and tendentially increased the number of Treg in skin, without having an overall impact on disease burden. This work provides evidence for the anti-inflammatory and tolerogenic effect of Exo-101, which may be harnessed for the treatment of Th17-driven inflammatory skin diseases, such as psoriasis.

Differential expression of IFN-γ induced CXC chemokines IP-10 and MIG in inflammatory skin diseases

1998 ◽  
Vol 16 ◽  
pp. S186
Author(s):  
J. Flier ◽  
D.M. Boorsma ◽  
P.J. van Beek ◽  
T.J. Stoof ◽  
R. Willemze ◽  
...  
Keyword(s):  
Differential Expression ◽  
Skin Diseases ◽  
Inflammatory Skin Diseases ◽  
Ifn Γ ◽  
Inflammatory Skin

scholarly journals Anti-Inflammatory Activity of a Medicinal Herb Extract Mixture, HM-V, on an Animal Model of DNCB-Induced Chronic Skin Inflammation

Plants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1546
Author(s):  
Sungbae Park ◽  
Sangmin Lee ◽  
Youngho Weon ◽  
Taewook Kim ◽  
Hakwon Kim ◽  
...  
Keyword(s):  
Animal Model ◽  
Inflammatory Cytokines ◽  
Skin Diseases ◽  
Skin Inflammation ◽  
Medicinal Herb ◽  
Inflammatory Skin Diseases ◽  
Tnf Α ◽  
Ifn Γ ◽  
Chronic Skin ◽  
Pro Inflammatory Cytokines

Chronic inflammatory skin diseases, such as atopic dermatitis, are caused by the accumulation of immune cells and the overproduction of chemokines, including CCL17 and CCL22, due to the activation of pro-inflammatory cytokines secreted from keratinocytes. In the present study, the inhibitory activity of HM-V on tumor necrosis factor alpha (TNF-α)/interferon gamma (IFN-γ)-induced pro-inflammatory cytokines was examined in human keratinocytes (HaCaTs) and 2,4-dinitrofluorobenzene (DNCB)-induced chronic skin contact dermatitis animal models. Traditional Asian medicinal herb extracts mixture (HM-V), which have been extensively used in Asian medicine, were utilized. In TNF-α/IFN-γ-induced HaCaTs, HM-V strongly inhibited mRNA and protein expression of CCL17 and CCL22 in a concentration-dependent manner. The expression of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 was also inhibited. Therefore, localized administration of HM-V in the DNCB-induced animal model alleviated immune cell deposition and skin inflammation. The results indicate that HM-V exerts inhibitory effects on keratinocyte production of CCL17 and CCL22. Furthermore, HM-V may be a useful anti-inflammatory agent for the prevention and treatment of inflammatory skin diseases.

scholarly journals Traditional Herbal FormulaBanhasasim-tangExerts Anti-Inflammatory Effects in RAW 264.7 Macrophages and HaCaT Keratinocytes

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Seong Eun Jin ◽  
Hye-Sun Lim ◽  
Yeji Kim ◽  
Chang-Seob Seo ◽  
Sae-Rom Yoo ◽  
...  
Keyword(s):  
Skin Diseases ◽  
Raw 264.7 Cells ◽  
Prostaglandin E ◽  
Raw 264.7 ◽  
Hacat Cells ◽  
Hacat Keratinocytes ◽  
Inflammatory Skin Diseases ◽  
Raw 264.7 Macrophages ◽  
Keratinocyte Cell ◽  
Anti Inflammatory

Banhasasim-tang(BHSST) is a Korean traditional herbal formula comprising eight medicinal herbs. The aim of the present study was to investigate the anti-inflammatory effect of BHSST using macrophage and keratinocyte cell lines. First, we evaluated the effects of BHSST on inflammatory mediator and cytokine production in lipopolysaccharide- (LPS-) stimulated RAW 264.7 macrophages. BHSST markedly inhibited the production of nitric oxide (NO), prostaglandin E2(PGE2), and interleukin- (IL-) 6. BHSST significantly suppressed the protein expression of toll-like receptor 4 (TLR4) and phosphorylated nuclear factor-kappa B (NF-κB) p65 in RAW 264.7 cells. Second, we examined whether BHSST influences the production of chemokines and STAT1 phosphorylation in tumor necrosis factor-α/interferon-γTI-stimulated HaCaT keratinocytes. BHSST significantly suppressed the production of RANTES/CCL5, TARC/CCL17, MDC/CCL22, and IL-8 in TI-stimulated HaCaT cells. BHSST also suppressed TI-induced phosphorylation of STAT1 in HaCaT cells. These results suggest that BHSST may be useful as an anti-inflammatory agent, especially for inflammatory skin diseases.

scholarly journals Microalgae as Potential Anti-Inflammatory Natural Product Against Human Inflammatory Skin Diseases

2020 ◽  
Vol 11 ◽  
Author(s):  
Wu-Thong Choo ◽  
Ming-Li Teoh ◽  
Siew-Moi Phang ◽  
Peter Convey ◽  
Wei-Hsum Yap ◽  
...  
Keyword(s):  
Natural Product ◽  
Skin Diseases ◽  
Inflammatory Skin Diseases ◽  
Inflammatory Skin ◽  
Anti Inflammatory

scholarly journals The Role of Gut Microbiome in Psoriasis: Oral Administration of Staphylococcus aureus and Streptococcus danieliae Exacerbates Skin Inflammation of Imiquimod-Induced Psoriasis-Like Dermatitis

2020 ◽  
Vol 21 (9) ◽  
pp. 3303 ◽  
Author(s):  
Karin Okada ◽  
Yoshiaki Matsushima ◽  
Kento Mizutani ◽  
Keiichi Yamanaka
Keyword(s):  
Gut Microbiome ◽  
Skin Diseases ◽  
Skin Inflammation ◽  
Gut Bacteria ◽  
Rrna Gene ◽  
Skin Microbiome ◽  
Inflammatory Skin Diseases ◽  
Fecal Microbiome ◽  
Tnf Α ◽  
Inflammatory Skin

Psoriasis is one of the common chronic inflammatory skin diseases in which inflammatory cytokines such as IL-17 and TNF-α play critical roles. Skin microbiome of psoriasis patients is reported to have elevated Staphylococcus and Streptococcus genus. There are controversial reports about gut microbiome of psoriasis patients, and whether the diversity of bacteria in genus level is decreased or not is still unclear. Moreover, it is not yet known if these gut bacteria would be the cause of the inflammation or the result of the inflammation. We analyzed the gut microbiome of the inflammatory skin model mouse (keratinocyte-specific caspase-1 transgenic (Kcasp1Tg) mouse), by analyzing the 16S rRNA gene. Staphylocuccus aureus and Streptococcus danieliae were abundant in Kcasp1Tg mouse fecal microbiome. These dominant bacteria as well as recessive control bacteria were orally administrated to antibiotic-treated wild type mice, and set up imiquimod-induced psoriasis-like skin inflammation model. The skin inflammation including ear thickness and histopathological findings was analyzed. The exacerbated skin lesions with the elevated levels of TNF-α, IL-17A, IL-17F, and IL-22 were observed in Staphylocuccus aureus and Streptococcus danieliae administrated groups. Our finding suggests that there is affinity between skin inflammation severity and certain gut bacteria leading to a vicious cycle: skin inflammation populates certain gut bacteria which itself worsens the skin inflammation. This is the first report on Staphylocuccus aureus and Streptococcuus danieliae effects in vivo. Not only treating the skin lesion but also treating the gut microbiome could be the future key treatment for inflammatory skin disease such as psoriasis.

scholarly journals Angiogenesis in Chronic Inflammatory Skin Disorders

2021 ◽  
Vol 22 (21) ◽  
pp. 12035
Author(s):  
Hyun Ji Lee ◽  
Yong Jun Hong ◽  
Miri Kim
Keyword(s):  
Growth Factor ◽  
Mast Cells ◽  
Transforming Growth Factor ◽  
Skin Diseases ◽  
Angiogenic Factor ◽  
Binding Motif ◽  
Interleukin 17 ◽  
Skin Disorders ◽  
Inflammatory Skin Diseases ◽  
Inflammatory Skin

Angiogenesis, the growth of new blood vessels from preexisting vessels, is associated with inflammation in various pathological conditions. Well-known angiogenetic factors include vascular endothelial growth factor (VEGF), angiopoietins, platelet-derived growth factor, transforming growth factor-β, and basic fibroblast growth factor. Yes-associated protein 1 (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) have recently been added to an important angiogenic factor. Accumulating evidence indicates associations between angiogenesis and chronic inflammatory skin diseases. Angiogenesis is deeply involved in the pathogenesis of psoriasis. VEGF, angiopoietins, tumor necrosis factor-a, interleukin-8, and interleukin-17 are unregulated in psoriasis and induce angiogenesis. Angiogenesis may be involved in the pathogenesis of atopic dermatitis, and in particular, mast cells are a major source of VEGF expression. Angiogenesis is an essential process in rosacea, which is induced by LL-37 from a signal cascade by microorganisms, VEGF, and MMP-3 from mast cells. In addition, angiogenesis by increased VEGF has been reported in chronic urticaria and hidradenitis suppurativa. The finding that VEGF is expressed in inflammatory skin lesions indicates that inhibition of angiogenesis is a useful strategy for treatment of chronic, inflammatory skin disorders.

Monoammonium glycyrrhizate suppresses tumor necrosis factor-α induced chemokine production in HMEC-1 cells, possibly by blocking the translocation of nuclear factor-κB into the nucleus

2014 ◽  
Vol 92 (10) ◽  
pp. 859-865 ◽  
Author(s):  
Na Cao ◽  
Tao Chen ◽  
Zai-pei Guo ◽  
Sha Qin ◽  
Meng-meng Li
Keyword(s):  
Tumor Necrosis ◽  
Skin Diseases ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Inflammatory Skin Diseases ◽  
Chemokine Production ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Necrosis Factor

Monoammonim glycyrrhizate (MAG) derived from licorice has been shown to have anti-inflammatory properties. Chemokines are vital inflammatory mediators that are involved with endothelial damage from leukocyte infiltrates in various inflammatory skin diseases. In this study, we investigated the anti-inflammatory effects and mechanisms of MAG on tumor necrosis factor-α (TNF-α) induced chemokine production in a human dermal microvascular endothelial cell line (HMEC-1). HMEC-1 cells were treated with TNF-α, with or without MAG. The results showed that MAG suppressed TNF-α-induced chemokine (including CXCL8, CX3CL1, and CXCL16) mRNA expression in HMEC-1 cells, in a dose-dependent manner, and reduced the secretion of these chemokines in culture supernatant. Moreover, endothelial activation in the presence of MAG blocked the chemotactic activities of TNF-α-stimulated HMEC-1 cell supernatant on the migration of primary neutrophils and primary monocytes. In addition, Western blot and immunofluorescence data revealed that MAG inhibited nuclear translocation of nuclear factor-κB p65 (NF-κB p65). It is the first report to demonstrate that MAG suppresses TNF-α-induced chemokine production in HMEC-1 cells, and that the mechanism may be inhibiting the translocation of NF-κB p65 into the nucleus to prevent the starting of inflammatory signaling pathway. Our results revealed that MAG is a potential anti-inflammatory agent capable of improving inflammatory skin diseases.

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