scholarly journals Rhododendron album Blume extract inhibits TNF-α/IFN-γ-induced chemokine production via blockade of NF-κB and JAK/STAT activation in human epidermal keratinocytes

2018 ◽  
Author(s):  
Ji‑Won Park ◽  
Han‑Sol Lee ◽  
Yourim Lim ◽  
Jin‑Hyub Paik ◽  
Ok‑Kyoung Kwon ◽  
...  
Keyword(s):  
Epidermal Keratinocytes ◽  
Human Epidermal Keratinocytes ◽  
Chemokine Production ◽  
Tnf Α ◽  
Ifn Γ

scholarly journals Up-regulation of Interferon-inducible protein 16 contributes to psoriasis by modulating chemokine production in keratinocytes

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Tianyu Cao ◽  
Shuai Shao ◽  
Bing Li ◽  
Liang Jin ◽  
Jie Lei ◽  
...  
Keyword(s):  
Critical Role ◽  
Underlying Mechanism ◽  
Epidermal Keratinocytes ◽  
Epidermal Hyperplasia ◽  
Chemokine Production ◽  
Stat3 Signaling ◽  
Tnf Α ◽  
Ifn Γ ◽  
Inducible Protein ◽  
Interferon Inducible Protein

Abstract Psoriasis is a common chronic inflammatory skin disease characterized by epidermal hyperplasia and dermal inflammation. Keratinocyte activation is known to play a critical role in psoriasis, but the underlying mechanism remains unclear. Interferon-inducible protein 16 (IFI16), an innate immune system sensor, is reported to affect keratinocyte function. We therefore hypothesized that IFI16 promotes psoriasis by modulating keratinocyte activation. In the present study, we cinfirmed that IFI16 was overexpressed in epidermal keratinocytes of psoriasis patients. In addition, psoriasis-related cytokines, including IFN-γ, TNF-α, IL-17 and IL-22, induced IFI16 up-regulation in keratinocytes via activation of STAT3 signaling. We also observed that IFI16 activated the TBK1-NF-κB signaling, leading to the production of CXCL10 and CCL20. Importantly, knocking down p204, which is reported as the mouse orthologous of human IFI16, inhibited epidermal hyperplasia in mice with imiquimod-induced psoriasiform dermatitis. These findings indicate that IFI16 plays a critical role in the pathogenesis of psoriasis and may be a potential therapeutic target.

scholarly journals Elevated IL-22 in psoriasis plays an anti-apoptotic role in keratinocytes through mediating Bcl-xL/Bax

APOPTOSIS ◽  
2020 ◽  
Vol 25 (9-10) ◽  
pp. 663-673
Author(s):  
Bo Wang ◽  
Dan Han ◽  
Fei Li ◽  
Weikun Hou ◽  
Lijuan Wang ◽  
...  
Keyword(s):  
Epidermal Keratinocytes ◽  
Healthy Controls ◽  
Human Epidermal Keratinocytes ◽  
Lesional Skin ◽  
Tnf Α ◽  
Proliferation And Apoptosis ◽  
Apoptotic Effect ◽  
Ifn Γ ◽  
Mediate Inflammation ◽  
Psoriatic Lesions

Abstract IL-22 is known to mediate inflammation in psoriasis, while IL-22 binding protein (IL-22BP) binds IL-22 to suppress IL-22 signaling. However, the function of IL-22 in regulating apoptosis in psoriasis remains poorly understood. In this study, we found that IL-22/IL-22R1 in lesional skin and IL-22 in serum from psoriatic patients were highly upregulated compared with healthy controls, while IL-22BP was not changed. Correlations between IL-22/IL-22R1 levels and the thickness of psoriatic lesions suggested that IL-22 might positively regulate abnormal hyperplasia in psoriasis. Apoptotic keratinocytes were increased only in stratum corneum, but not in spinous and basal layers of psoriasis. Moreover, IL-22 promoted cell viability in human epidermal keratinocytes (HEKs). The apoptosis induced by TNF-α and IFN-γ was inhibited in HEKs treated with IL-22, since that IL-22 upregulated Bcl-xL and downregulated Bax production in HEKs in the presence of TNF-α and IFN-γ. In addition, IL-22BP could counteract the anti-apoptotic effect of IL-22. Our finding demonstrates that IL-22 might play an anti-apoptosis role on keratinocytes to balance cell proliferation and apoptosis in psoriatic epidermis.

scholarly journals Impressic Acid Ameliorates Atopic Dermatitis-Like Skin Lesions by Inhibiting ERK1/2-Mediated Phosphorylation of NF-κB and STAT1

2021 ◽  
Vol 22 (5) ◽  
pp. 2334
Author(s):  
Jae Ho Choi ◽  
Gi Ho Lee ◽  
Sun Woo Jin ◽  
Ji Yeon Kim ◽  
Yong Pil Hwang ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Skin Lesions ◽  
Histopathological Analysis ◽  
Mrna Levels ◽  
Chemokine Production ◽  
Dermal Thickness ◽  
Skin Symptoms ◽  
Tnf Α ◽  
Ifn Γ ◽  
In Cells

Impressic acid (IPA), a lupane-type triterpenoid from Acanthopanax koreanum, has many pharmacological activities, including the attenuation of vascular endothelium dysfunction, cartilage destruction, and inflammatory diseases, but its influence on atopic dermatitis (AD)-like skin lesions is unknown. Therefore, we investigated the suppressive effect of IPA on 2,4-dinitrochlorobenzene (DNCB)-induced AD-like skin symptoms in mice and the underlying mechanisms in cells. IPA attenuated the DNCB-induced increase in the serum concentrations of IgE and thymic stromal lymphopoietin (TSLP), and in the mRNA levels of thymus and activation regulated chemokine(TARC), macrophage derived chemokine (MDC), interleukin-4 (IL-4), interleukin-5 (IL-5), interleukin-13 (IL-13), tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ) in mice. Histopathological analysis showed that IPA reduced the epidermal/dermal thickness and inflammatory and mast cell infiltration of ear tissue. In addition, IPA attenuated the phosphorylation of NF-κB and IκBα, and the degradation of IκBα in ear lesions. Furthermore, IPA treatment suppressed TNF-α/IFN-γ-induced TARC expression by inhibiting the NF-κB activation in cells. Phosphorylation of extracellular signalregulated protein kinase (ERK1/2) and the signal transducer and activator of transcription 1 (STAT1), the upstream signaling proteins, was reduced by IPA treatment in HaCaT cells. In conclusion, IPA ameliorated AD-like skin symptoms by regulating cytokine and chemokine production and so has therapeutic potential for AD-like skin lesions.

Retinoic Acid Potentiates TNF-α-Induced ICAM-1 Expression in Normal Human Epidermal Keratinocytes

1999 ◽  
Vol 255 (1) ◽  
pp. 64-69 ◽  
Author(s):  
Sophie Janssens ◽  
Luc Bols ◽  
Marc Vandermeeren ◽  
Guy Daneels ◽  
Marcel Borgers ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Epidermal Keratinocytes ◽  
Human Epidermal Keratinocytes ◽  
Normal Human Epidermal Keratinocytes ◽  
Tnf Α ◽  
Normal Human

scholarly journals Indirubin attenuates mouse psoriasis-like skin lesion in a CD274-dependent manner: an achievement of RNA sequencing

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Xiaochun Xue ◽  
Jianhua Wu ◽  
Junhui Li ◽  
Jianguo Xu ◽  
Haiying Dai ◽  
...  
Keyword(s):  
Network Analysis ◽  
Skin Lesion ◽  
Candidate Genes ◽  
Rna Sequencing ◽  
Molecular Mechanisms ◽  
Regulatory Mechanisms ◽  
Epidermal Keratinocytes ◽  
Dependent Manner ◽  
Human Epidermal Keratinocytes ◽  
Ifn Γ

It was previously reported that the expression of CD274 was down-regulated in psoriatic epidermis, leading to immune disorders of psoriasis. However, the regulatory mechanisms of CD274 were rarely elucidated. We aimed to explore the regulatory mechanisms of CD274. Skin samples were collected from 18 patients with psoriasis vulgaris and 9 healthy participants for RNA sequencing. Candidate genes were chosen based on degree and k-core difference of genes in the co-expression network. The relations between candidate genes and CD274 were validated by flow cytometry and real-time PCR in primary human epidermal keratinocytes. The therapeutic effect of indirubin was assessed in an imiquimod-treated mouse model. Interferon-γ (IFN-γ), cyclin-dependent kinase (CDK) 1, Toll-like receptor 3 (TLR3), TLR4 and interleukin (IL)-17A were considered as candidate genes. In primary human epidermal keratinocytes, the level of CD274 was obviously increased under the stimulation of IFN-γ and CDK1 inhibitor (indirubin), independent of TLR4, TLR3 or IL-17A. Indirubin alleviated the severity of psoriatic mice in a CD274-dependent manner. Co-expression network analysis served as an effective method for the exploration of molecular mechanisms. We demonstrated for the first time that CD274 was the regulator of indirubin-mediated effect on mouse psoriasis-like skin lesion based on co-expression network analysis, contributing to the alleviation of mouse psoriasis-like skin lesion.

scholarly journals Interleukin-8 and Tumor Necrosis Factor Alpha Production in Human Epidermal Keratinocytes Induced by Trichophyton mentagrophytes

2002 ◽  
Vol 9 (4) ◽  
pp. 935-937 ◽  
Author(s):  
Yuka Nakamura ◽  
Rui Kano ◽  
Atsuhiko Hasegawa ◽  
Shinichi Watanabe
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Trichophyton Mentagrophytes ◽  
Epidermal Keratinocytes ◽  
Human Epidermal Keratinocytes ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Production of interleukin-8 (IL-8) and tumor necrosis factor alpha (TNF-α) was confirmed by enzyme-linked immunosorbent assay in a medium where human epidermal keratinocytes were cocultured with Trichophyton mentagrophytes for 1 to 12 h. IL-8 and TNF-α mRNAs were also detected in the keratinocytes cocultured with T. mentagrophytes.

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