共查询到20条相似文献,搜索用时 31 毫秒
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Benjamin Frempah Lerin R. Luckett‐Chastain Randle M. Gallucci 《Experimental dermatology》2019,28(8):948-955
Irritant contact dermatitis (ICD) is characterized by epidermal hyperplasia, infiltration of leucocytes into lesional skin and inflammatory cytokine release. The cellular infiltrate during ICD comprises primarily cells of the myeloid lineage. Our group has previously shown that the cytokine IL‐6 confers a protective effect to lesional skin during ICD. How IL‐6Rα function in myeloid cells is involved in the inflammatory response during ICD is, however, unknown. In the present study, utilizing a chemical model of ICD, it is shown that mice with a myeloid‐specific knockout of the IL‐6Rα (IL‐6RαΔmyeloid) display an exaggerated inflammatory response to benzalkonium chloride (BKC) and Jet propellant‐8 (JP8) fuel, two well‐characterized irritants relative to littermate control. Results from immunohistochemical and flow cytometric analyses revealed that IL‐6RαΔmyeloid mouse skin displayed increased epidermal hyperplasia and inflammatory monocyte influx into lesional skin but lower numbers of resident macrophages relative to littermate controls after irritant exposure. Multiplex immunoassay revealed significantly higher levels of pro‐inflammatory cytokines IL‐1α and TNF‐α, but reduced expression of chemokine proteins including CCL2‐5, CCL7, CCL11, CXCL1 and CXCL10 in IL‐6RαΔmyeloid mouse skin relative to littermate control following irritant exposure. These results highlight a previously unknown role of IL‐6Rα function in myeloid cells in modulating the inflammatory response and myeloid population dynamics during ICD. 相似文献
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Yu‐Ping Hsiao Jen‐Hung Yang Wen‐Jun Wu Meng‐Hsuan Lin Gwo‐Tarng Sheu 《Experimental dermatology》2013,22(10):672-674
The lack of a human papillomavirus (HPV)‐infected skin cancer cell line has hampered the investigation of the interaction of UV and HPV in skin carcinogenesis. We identified a human basal cell carcinoma (BCC‐1/KMC) cell line integrated with E6 and E7 genes of high‐risk HPV type 18 and demonstrated that repression of E6 and E7 results in proliferation inhibition. Sublethal ultraviolet‐B (UVB) irradiation induced the expressions of interleukin‐6 (IL‐6) and interleukin‐8 (IL‐8), as well as viral E6 and E7 genes, in BCC‐1/KMC cells. When E6 and E7 expressions were inhibited, IL‐6/IL‐8 expressions were repressed. Furthermore, IL‐6/IL‐8 remained inducible by UVB irradiation when E6 and E7 were inhibited. These results indicated that IL‐6 and IL‐8 can be upregulated by viral E6 and E7 proteins without UVB irradiation. Moreover, chronic exposure to UVB upregulates IL‐6 and IL‐8 when E6/E7 is induced by UVB. 相似文献
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BackgroundGinseng has been known in Korea as a health-supportive herbal medicine from time immemorial. Essential oil isolated from fresh ginseng has been shown to display antibacterial and anti-inflammatory activities.ObjectiveThe effects of red ginseng oil (RGO) on the lipopolysaccharide (LPS)-treated sebocytes and outer root sheath (ORS) cells were studied.MethodsThe cultured cells were treated with either 0.1% dimethyl sulfoxide, 5 µg/ml LPS, 50 µg/ml RGO, or 5 µg/ml LPS plus 50 µg/ml RGO for 6 and 24 hours. RT-PCR, real-time PCR, enzyme-linked immunosorbent assay, western blot, and immunofluorescence staining were performed for the analysis of inflammatory cytokine.ResultsRGO showed the increased gene and protein expression of inflammatory cytokines, including interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α in the LPS-treated sebocytes and ORS cells. RGO also showed the increased protein expression of p-c-jun and p-JNK in the LPS-treated sebocytes and ORS cells. Gene expression of TLR2 was increased in LPS-treated sebocytes following treatment with RGO. Additionally, RGO resulted in an increased expression of LL-37 in the LPS-treated sebocytes and ORS cells. Moreover, it remarkably increased the production of sebum in LPS-treated sebocytes.ConclusionRGO might be among the aggravating factors of acne vulgaris. It would be better to stop taking red ginseng in patients with inflammatory acne. 相似文献
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Ji‐Young Bae Jung‐Suk Choi Sang‐Wook Kang Yong‐Jin Lee Jinseu Park Young‐Hee Kang 《Experimental dermatology》2010,19(8):e182-e190
Please cite this paper as: Dietary compound ellagic acid alleviates skin wrinkle and inflammation induced by UV‐B irradiation. Experimental Dermatology 2010; 19 : e182–e190. Abstract: Ellagic acid, a polyphenol compound present in berries and pomegranate, has received attention as an agent that may have potential bioactivities preventing chronic diseases. This study examined photoprotective effects of ellagic acid on collagen breakdown and inflammatory responses in UV (ultraviolet)‐B irradiated human skin cells and hairless mice. Ellagic acid attenuated the UV‐B‐induced toxicity of HaCaT keratinocytes and human dermal fibroblasts. Non‐toxic ellagic acid markedly prevented collagen degradation by blocking matrix metalloproteinase production in UV‐B‐exposed fibroblasts. Anti‐wrinkle activity of ellagic acid was further investigated in hairless mice exposed to UV‐B, in which it attenuated UV‐B‐triggered skin wrinkle formation and epidermal thickening. Topical application of 10 μmol/l ellagic acid diminished production of pro‐inflammatory cytokines IL‐1β and IL‐6, and blocked infiltration of inflammatory macrophages in the integuments of SKH‐1 hairless mice exposed to UV‐B for 8 weeks. In addition, this compound mitigated inflammatory intracellular cell adhesion molecule‐1 expression in UV‐B‐irradiated keratinocytes and photoaged mouse epidermis. These results demonstrate that ellagic acid prevented collagen destruction and inflammatory responses caused by UV‐B. Therefore, dietary and pharmacological interventions with berries rich in ellagic acid may be promising treatment strategies interrupting skin wrinkle and inflammation associated with chronic UV exposure leading to photoageing. 相似文献
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Nograles KE Zaba LC Guttman-Yassky E Fuentes-Duculan J Suárez-Fariñas M Cardinale I Khatcherian A Gonzalez J Pierson KC White TR Pensabene C Coats I Novitskaya I Lowes MA Krueger JG 《The British journal of dermatology》2008,159(5):1092-1102
Background Psoriasis vulgaris is an inflammatory skin disease mediated by Th1 and Th17 cytokines, yet the relative contribution of interferon (IFN)‐γ, interleukin (IL)‐17 and IL‐22 on disease pathogenesis is still unknown. Objectives In this study, we sought to identify the cytokines produced by skin‐resident T cells in normal skin, localize the receptors for these cytokines, and examine how these cytokines alter gene expression profiles of the cells bearing cognate receptors. Methods We used intracellular cytokine staining and flow cytometry to evaluate T cell cytokine production, and immunohistochemistry and double‐label immunofluorescence to localize cytokine receptors in skin. Gene array analysis of cytokine‐treated keratinocytes was performed using moderated paired t‐test controlling for false discovery rate using the Benjamini–Hochberg procedure. Results We demonstrate that T‐helper cells producing IL‐17, IL‐22 and/or IFN‐γ, as well as the cells bearing cognate cytokine receptors, are present in normal human skin. Keratinocytes stimulated with IL‐17 expressed chemokines that were different from those induced by IFN‐γ, probably contributing to the influx of neutrophils, dendritic cells and memory T cells into the psoriatic lesion. In contrast, IL‐22 downregulated genes associated with keratinocyte differentiation and caused epidermal alterations in an organotypic skin model. Conclusions Our results suggest that the Th17 cytokines IL‐17 and IL‐22 mediate distinct downstream pathways that contribute to the psoriatic phenotype: IL‐17 is more proinflammatory, while IL‐22 retards keratinocyte differentiation. 相似文献
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The immunological characterization in the pathogenesis of urticaria, mainly regarding cytokine profile, needs more investigation. In this study, subgroups of the T, B and natural killer (NK) lymphocyte from peripheral blood and serum levels of interleukin (IL)‐15, IL‐21 and immunoglobulin (Ig)E were examined in patients with acute urticaria (AU) and chronic urticaria (CU). Moreover, symptom scores and course of the patients were assessed. The percentage of NK cells and the ratio of CD4+/CD8+ increased, however, CD8+ decreased in CU compared to controls (P < 0.01). But no significant changes of T, B and NK lymphocyte were found in AU. IL‐15 and IL‐21 significantly decreased in AU and CU, but IgE increased. CU with a positive autologous serum skin test were more likely to be associated with longer course and higher CD3+, B cells and IL‐21, and lower IgE (P < 0.01). Weak negative correlations were demonstrated between CD3+, CD8+ and scores in CU (r = ?0.23, ?0.25, P < 0.05). Significant correlations were found between B cells and scores and course in CU (r = 0.49, 0.65, P < 0.01). Moreover, a significant correlation was found between IL‐21 and IgE (r = 0.42, P < 0.01) in CU. But no significant correlations were found in AU. Our findings supported the concept that both humoral immunity and cellular immunity dysregulation in the pathogenesis of urticaria – mainly related to the decrease of the serum levels of IL‐15 and IL‐21 – may induce the increasing expression of IgE produced by B cells. 相似文献
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MinJeong Kim Ju Hee Kim Guk Jin Jeong Kui Young Park Mi‐Kyung Lee Seong Jun Seo 《Experimental dermatology》2019,28(7):809-815
Particulate matter (PM) is known to have harmful effects on human health. Epidemiological studies have suggested that PM exposure is related to skin diseases and extrinsic skin ageing. However, the mechanisms by which PM affects skin are unclear. The aim of this study was to investigate the mechanism of action of PMs on epidermal inflammation and skin ageing using a co‐culture of human keratinocytes (HaCaT) and fibroblasts (HDF). SRM 1648a (pmA) and 1649b (pmB), which mainly comprise heavy metals and polycyclic aromatic hydrocarbons, respectively, were used as reference PMs. Cytotoxic effects, activation of AhR, phosphorylation of p38 kinase and ROS generation were examined in PM‐treated HaCaT cells. The phosphorylation of p38 MAPK induced by PMs was shown to be critically important for the increases in IL‐1α and IL‐1β expression. Moreover, the mRNA and protein expression levels of MMP1 and COX2 were markedly increased in HDF cells co‐cultured with PM‐treated HaCaT cells. In conclusion, PMs induce the expression of pro‐inflammatory cytokines in keratinocytes via the p38 MAPK pathway, and these interleukins increase the expression of MMP1 and COX2 in HDF cells. These results suggest that PMs trigger skin ageing via p38 MAPK activation and interleukin secretion in epidermal keratinocytes. 相似文献
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Increased expression of IL‐33 in rosacea skin and UVB‐irradiated and LL‐37‐treated HaCaT cells
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Eunah Suhng Bo Hee Kim You Won Choi Hae Young Choi Hyunjin Cho Ji Yeon Byun 《Experimental dermatology》2018,27(9):1023-1029
Rosacea is one of the most common dermatoses of adults. Although the detailed pathophysiology remains unknown, it is thought that rosacea is caused by a consistently aberrant, innate immune response, and that LL‐37 plays an important role. However, involvement of the inflammatory cytokine IL‐33 has not yet been studied. We explored the role played by IL‐33 in the pathophysiology of rosacea. First, we immunohistochemically evaluated the expression of IL‐33 and its receptor (ST2) in rosacea skin. Second, we exposed HaCaT cells to ultraviolet B (UVB) irradiation in the presence or absence of LL‐37 and measured the expression of proinflammatory cytokines including IL‐33. We also analysed VEGF (vascular endothelial growth factor) mRNA expression and protein release after costimulation of HaCaT cells by LL‐37 and IL‐33. Immunohistochemically, IL‐33 expression was enhanced in the skin of rosacea patients, especially with erythematotelangiectatic subtype. In vitro, UVB and LL‐37 synergistically increased mRNAs expression of proinflammatory cytokines, especially IL‐33 and IL‐1β. IL‐33 protein release was also synergistically increased by LL‐37 and UVB treatment. LL‐37 and IL‐33 stimulated VEGF mRNA expression and VEGF release from HaCaT cells. Our findings suggest that rosacea skin with abundant LL‐37 may robustly produce and release IL‐33 when exposed to UV radiation. IL‐33 may participate in the angiogenesis and vasodilation of rosacea skin by enhancing VEGF release. 相似文献
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Yu-Ra Jung Jung-Min Shin Chang-Hyeon Kim Sooil Kim Chang-Deok Kim Young-Joon Seo Jeung-Hoon Lee Myung Im Young Lee Young Ho Lee 《ANNALS OF DERMATOLOGY》2021,33(6):541
BackgroundSebocytes are the main cells involved in the pathogenesis of acne by producing lipids and inflammatory cytokines. Although palmitic acid (PA) has been suggested to induce an inflammatory reaction, its effect on sebocytes remains to be elucidated.ObjectiveIn the present study, we investigated whether PA promotes inflammasome-mediated inflammation of sebocytes both in vivo and in vitro.MethodsWe intradermally injected PA into the mice ears. And, we treated cultured human sebocytes with PA. Inflammasome-mediated inflammation was verified by immunohistochemistry, Western blot and ELISA.ResultsPA-treated mice developed an inflammatory response associated with increased interleukin (IL)-1β expression in the sebaceous glands. When PA was added to cultured human sebocytes, caspase-1 activation and IL-1β secretion were significantly enhanced. In addition, NLRP3 knockdown attenuated IL-1β production by sebocytes stimulated with PA. PA-mediated inflammasome activation required reactive oxygen species.ConclusionThese findings indicate that PA activates the NLRP3 inflammasome before induction of an inflammatory response in sebocytes. Thus, PA may play a role in the inflammation of acne. 相似文献
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Please cite this paper as: NF‐κB is involved in inhibition of lipoxin A4 on dermal inflammation and hyperplasia induced by mezerein. Experimental Dermatology 2010; 19 : e286–e288. Abstract: The mechanisms by which lipoxin A4 (LXA4) inhibit skin inflammation remain unclear. In the present studies, the ear inflammatory model was induced by topical application of mezerein. Treatment of the mouse ear with LXA4 exhibited the inhibitory effects on oedema, neutrophil infiltration, vascular permeability, expressions of interleukin (IL)‐1, IL‐6 and IL‐8 mRNA, DNA‐binding activity of nuclear factor‐κB (NF‐κB), and on dermal hyperplasia. NF‐κB reporter activities and nuclear translocations of NF‐κB p65 in cultured keratinocytes stimulated by mezerein were inhibited by pretreatment of the cells with LXA4. LXA4 reduced degradation, but not phosphorylation of IκBα in cultured keratinocytes stimulated by mezerein, suggesting that LXA4‐attenuated IκBα degradation may restore the mezerein‐blocked inhibitory effects of IκB on nuclear translocation and DNA‐binding activity of NF‐κB. Our results demonstrated that LXA4 displays the anti‐inflammatory and anti‐proliferative role on ear inflammatory model induced by mezerein and these effects were related with downregulation of DNA‐binding activity of NF‐κB. 相似文献
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G. Monfrecola F. Gaudiello T. Cirillo G. Fabbrocini A. Balato S. Lembo 《Clinical and experimental dermatology》2013,38(2):185-188
Ultraviolet (UV) radiation has profound effects on human skin, causing sunburn, inflammation, cellular‐tissue injury, cell death, and skin cancer. Most of these effects are mediated by a number of cytokines produced by keratinocytes. In this study we investigated whether nicotinamide (NCT), the amide form of vitamin B3, might have a protective function in reducing the expression of interleukin (IL)‐1β, IL‐6, IL‐8, IL‐10, monocyte chemoattractant protein (MCP)‐1 and tumour necrosis factor (TNF)‐α in UV‐irradiated keratinocytes. HaCaT cells were treated with UVB in the presence or absence of NCT, and cytokine mRNA levels were examined by quantitative real‐time PCR. NCT significantly downregulated IL‐6, IL‐10, MCP‐1 and TNF‐α mRNA expression, whereas it did not exert any significant effect on IL‐1β or IL‐8 expression. Because of its ability to decrease these cytokine mediators after UV exposure, NCT is a possible therapy to improve or prevent conditions induced or aggravated by UV light. 相似文献
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Dóra Kovács Marianna Lovászi Szilárd Póliska Attila Oláh Tamás Bíró Imre Veres Christos C. Zouboulis Mona Ståhle Ralph Rühl Éva Remenyik Dániel Törőcsik 《Experimental dermatology》2016,25(3):194-199
In addition to producing sebum, sebocytes link lipid metabolism with inflammation at a cellular level and hence, greatly resemble adipocytes. However, so far no analysis was performed to identify and characterize the adipocyte‐associated inflammatory proteins, the members of the adipokine family in sebocytes. Therefore, we determined the expression profile of adipokines [adiponectin, interleukin (IL) 6, resistin, leptin, serpin E1, visfatin, apelin, chemerin, retinol‐binding protein 4 (RBP4) and monocyte chemoattractant protein 1 (MCP1)] in sebaceous glands of healthy and various disease‐affected (acne, rosacea, melanoma and psoriasis) skin samples. Sebaceous glands in all examined samples expressed adiponectin, IL6, resistin, leptin, serpin E1 and visfatin, but not apelin, chemerin, RBP4 and MCP1. Confirming the presence of the detected adipokines in the human SZ95 sebaceous gland cell line we further characterized their expression and secretion patterns under different stimuli mimicking bacterial invasion [by using Toll‐like receptor (TLR)2 and 4 activators], or by 13‐cis retinoic acid (13CRA; also known as isotretinoin), a key anti‐acne agent. With the exception of resistin, the expression of all of the detected adipokines (adiponectin, IL6, leptin, serpin E1 and visfatin) could be further regulated at the level of gene expression, showing a close correlation with the secreted protein levels. Besides providing further evidence on similarities between adipocytes and sebocytes, our results strongly suggest that sebocytes are not simply targets of inflammation but may exhibit initiatory and modulatory roles in the inflammatory processes of the skin through the expression and secretion of adipokines. 相似文献
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Weon Ju Lee Hong Dae Jung Seong Geun Chi Byung Soo Kim Seok-Jong Lee Do Won Kim Moon Kyu Kim Jung Chul Kim 《Archives of dermatological research》2010,302(6):429-433
Acne is a complex, chronic and common skin disorder of pilosebaceous units. Hyperkeratinization of keratinocytes, increased
sebum excretion from sebocytes via androgen stimulation and inflammatory cytokines are the major factors involved in the pathophysiology
of acne. In addition, it is known that keratinocytes play an important role in acne synthesizing a number of inflammatory
cytokines. However, the nature of the association between inflammatory cytokines and sebocytes in acne remains unclear. Culture
of sebocytes provides a new insight into the participation of dihydrotestosterone (DHT) in the production of inflammatory
cytokines in acne. To examine the possible involvement of DHT in the production of inflammatory cytokines in the cultured
sebocytes, we used immunohistochemistry and RT-PCR to compare the expression of interleukin-1 (IL-1), IL-6, tumor necrosis
factor-α (TNF-α). Upregulation of IL-6 and TNF-α in immunohistochemistry, and increase in RNA amplification for IL-6 and TNF-α
were observed after addition of DHT compared with the control. This study suggests that DHT may not only be involved in sebum
production but also in production of proinflammatory cytokines in acne. 相似文献
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Supriya Bhardwaj Alka Bhatia Muthu Sendhil Kumaran Davinder Parsad 《Experimental dermatology》2019,28(6):682-689
Cytokines regulate immune response and inflammation and play an important role in depigmentation process of an autoimmune disease, vitiligo. We sought to determine how inflammatory cytokines influence the progression of vitiligo, and based on that, we develop a logical therapeutic intervention using primary melanocyte culture. Melanocytes were cultured and exposed to IL‐17A, IL‐1β, IFN‐γ and TGF‐β for 4 days. Melanocytes proliferation, tyrosinase assay and melanin content were measured. Real‐Time PCR was used to analyse mRNA expression of genes specific for melanocytes growth and pigmentation. Anti‐IL‐17A receptor antibody was used to block IL‐17A receptors expressed on melanocytes. Protein expression of MITF and TYR was assessed by immunofluorescence and Western blotting. A gradual decline in the melanocyte population, melanin content and tyrosinase activity was observed after different cytokine treatment. The expression of MITF and its downstream genes after blocking with anti‐IL‐17RA, an increased melanin content, increased expression of TYR, MITF along with its downstream genes, and cell proliferation was observed. 相似文献
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Shan Jin Chang Ook Park Jung U Shin Ji Yeon Noh Yun Sun Lee Na Ra Lee Hye Ran Kim Seongmin Noh Young Lee Jeung‑Hoon Lee Kwang Hoon Lee 《Experimental dermatology》2014,23(12):938-941
S100A9 and S100A8 are called damage‐associated molecular pattern (DAMP) molecules because of their pro‐inflammatory properties. Few studies have evaluated S100A9 and S100A8 function as DAMP molecules in atopic dermatitis (AD). We investigated how house‐dust mites affect S100A9 and S100A8 expression in Th2 cytokine‐ and Th17 cytokine‐treated keratinocytes, and how secretion of these molecules affects keratinocyte‐derived cytokines. Finally, we evaluated expression of these DAMP molecules in AD patients. S100A9 expression and S100A8 expression were strongly induced in IL‐17A‐ and Dermatophagoides (D.) farinae‐treated keratinocytes, respectively. Furthermore, co‐treatment with D. farinae and IL‐17A strongly increased expression of S100A9 and S100A8 compared with D. farinae‐Th2 cytokine co‐treatment. The IL‐33 mRNA level increased in a dose‐dependent manner in S100A9‐treated keratinocytes, but TSLP expression did not change. S100A8/A9 levels were also higher in the lesional skin and serum of AD patients, and correlated with disease severity. Taken together, S100A9 and S100A8 may be involved in inducing DAMP‐mediated inflammation in AD triggered by IL‐17A and house‐dust mites. 相似文献
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Increasing evidence suggests that human epidermal melanocytes play an important role in the skin immune system; however, a role of their pigmentation in immune and inflammatory responses is poorly examined. In the study, the expression of Toll‐like receptor 4 (TLR4) and inflammatory cytokines and chemokines by cultured normal melanocytes derived from lightly and darkly pigmented skin was investigated after cell stimulation with lipopolysaccharide (LPS). The basal TLR4 mRNA level in heavily pigmented cells was higher as compared to their lightly pigmented counterparts. Melanocyte exposure to LPS upregulated the expression of TLR4 mRNA and enhanced the DNA‐binding activity of NF‐κB p50 and p65. We found substantial differences in the LPS‐stimulated expression of numerous genes encoding inflammatory cytokines and chemokines between the cells with various melanin contents. In lightly pigmented melanocytes, the most significantly upregulated genes were nicotinamide phosphoribosyltransferase (NAMPT/visfatin), the chemokines CCL2 and CCL20, and IL6, while the genes for CXCL12, IL‐16 and the chemokine receptor CCR4 were the most significantly upregulated in heavily pigmented cells. Moreover, the lightly pigmented melanocytes secreted much more NAMPT, CCL2 and IL‐6. The results of our study suggest modulatory effect of melanogenesis on the immune properties of normal epidermal melanocytes. 相似文献