• 제목/요약/키워드: Interleukin-17

검색결과 235건 처리시간 0.029초

Effect of Cordycepin on the Expression of the Inflammatory Cytokines TNF-alpha, IL-6, and IL-17A in C57BL/6 Mice

  • Seo, Min Jeong;Kim, Min Jeong;Lee, Hye Hyeon;Park, Jeong Uck;Kang, Byoung Won;Kim, Gi-Young;Rhu, En Ju;Kim, Jung-In;Kim, Kwang Hyuk;Jeong, Yong Kee
    • Journal of Microbiology and Biotechnology
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    • 제23권2호
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    • pp.156-160
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    • 2013
  • Culture supernatants of splenocytes from C57BL/6 mice were exposed to 0.3, 1.0, and 3.0 ${\mu}g/ml$ cordycepin plus 3.0 ${\mu}g/ml$ lipopolysaccharide (LPS) to investigate the effects of cordycepin (3'-deoxyadenosine) on the production of inflammatory cytokines. Coadministration of 3.0 ${\mu}g/ml$ cordycepin with LPS in cultured murine spleen cells significantly diminished expression of the inflammatory cytokines tumor necrosis factor-${\alpha}$ and interleukin-6 (IL-6) in a time-dependent manner. Expression of the inflammatory cytokine IL-17A was substantially downregulated in a timeand concentration-dependent manner at all cordycepin concentrations. These findings suggest that cordycepin downregulates the immediate hypersensitivity reaction stimulated by LPS.

Association of miR-1266 with Recurrence/Metastasis Potential in Estrogen Receptor Positive Breast Cancer Patients

  • Sevinc, Elif Demirdogen;Egeli, Unal;Cecener, Gulsah;Tezcan, Gulcin;Tunca, Berrin;Gokgoz, Sehsuvar;Tasdelen, Ismet;Tolunay, Sahsine;Evrensel, Turkkan
    • Asian Pacific Journal of Cancer Prevention
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    • 제16권1호
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    • pp.291-297
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    • 2015
  • The Homeobox B13 (HOXB13):Interleukin 17 Receptor B (IL17BR) index of estrogen receptor (ER)-positive breast cancer (ER (+) BC) patients may be a potential biomarker of recurrence/ metastasis. However, effects of microRNA (miRNA) binding to the 3' untranslated region (3' UTR) of HOXB13 and IL17BR and its function on recurrence/metastasis in ER (+) BC remains elusive. The aims of this study were to determine the expression of miRNAs that bind to 3' UTR of HOXB13 and IL17BR in ER (+) BC patients and asess the effects of these miRNAs on recurrence/metastasis. The expression profiles of HOXB13 and IL17BR were evaluated using RT-PCR in tumors and normal tissue samples from 40 ER (+) BC patients. The expression level of 4 miRNAs, which were predicted to bind the 3' UTR of HOXB13 and IL17BR using TargetScan, microRNA.org and miRDB online databases, were further evaluated with RT-PCR. Our findings demonstrated that high miR-1266 levels might be significant prognostic factor for recurrence/metastasis occurrence (3.05 fold p=0.004) and tamoxifen response (3.90 fold; p=0.2514) in ER (+) BC cases. Although we suggest that modulation of miR-1266 expression may be an important mechanism underlying the chemoresistance of ER (+) BC, advanced studies and validation are required.

IL-17 and IL-17C Signaling Protects the Intestinal Epithelium against Diisopropyl Fluorophosphate Exposure in an Acute Model of Gulf War Veterans' Illnesses

  • Kristen M. Patterson;Tyler G. Vajdic;Gustavo J. Martinez;Axel G. Feller;Joseph M. Reynolds
    • IMMUNE NETWORK
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    • 제21권5호
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    • pp.35.1-35.16
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    • 2021
  • Gulf War Veterans' Illnesses (GWI) encompasses a broad range of unexplained symptomology specific to Veterans of the Persian Gulf War. Gastrointestinal (GI) distress is prominent in veterans with GWI and often presents as irritable bowel syndrome (IBS). Neurotoxins, including organophosphorus pesticides and sarin gas, are believed to have contributed to the development of GWI, at least in a subset of Veterans. However, the effects of such agents have not been extensively studied for their potential impact to GI disorders and immunological stability. Here we utilized an established murine model of GWI to investigate deleterious effects of diisopropyl fluorophosphate (DFP) exposure on the mucosal epithelium in vivo and in vitro. In vivo, acute DFP exposure negatively impacts the mucosal epithelium by reducing tight junction proteins and antimicrobial peptides as well as altering intestinal microbiome composition. Furthermore, DFP treatment reduced the expression of IL-17 in the colonic epithelium. Conversely, both IL-17 and IL-17C treatment could combat the negative effects of DFP and other cholinesterase inhibitors in murine intestinal organoid cells. Our findings demonstrate that acute exposure to DFP can result in rapid deterioration of mechanisms protecting the GI tract from disease. These results are relevant to suspected GWI exposures and could help explain the propensity for GI disorders in GWI Veterans.

Immunological mechanism of postherpetic neuralgia and effect of pregabalin treatment on the mechanism: a prospective single-arm observational study

  • Mercan, Aysel;Uzun, Sema Tuncer;Keles, Sevgi;Hacibeyoglu, Gulcin;Yilmaz, Resul;Reisli, Ruhiye
    • The Korean Journal of Pain
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    • 제34권4호
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    • pp.463-470
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    • 2021
  • Background: Although neuropathic pain is a severe and common pain, its pathophysiology has not been elucidated yet. Studies in recent years have focused on the immune system's role in the pathogenesis of neuropathic pain. The aim of this study was to investigate the role of immunological mechanisms in neuropathic pain and the effect of pregabalin by measuring immunological marker levels in peripheral blood before and after pregabalin treatment in postherpetic neuralgia (PHN) patients with neuropathic pain. Methods: Forty patients diagnosed with PHN were included in the study. CD4, T follicular cells (Tfh: CD4+CXCR5+PD1+), Th17 (CD4+CCR6+ and CD4+IL17A+), regulatory T cells (Treg: CD4+ CD25+foxp3+), Th1 (CD4+ CXCR3+ and CD4+ IFN-γ+) and Th2 (CD4+ IL-4+) cell ratios were measured in peripheral blood samples before treatment and after 3 months of treatment. Results: When immunological marker and inflammation parameter levels were compared before and after treatment, the helper T cell ratio (CD3+, CD4+) was 30.28 ± 12.27% before treatment and 34.93 ± 11.70% after treatment, so there was a statistically significant increase (P = 0.028). Th17 was 4.75 ± 5.02% before treatment and 5.80 ± 3.13% after treatment, and there was a statistically significant increase (P = 0.036). Conclusions: Immunological mechanisms play an essential role in the pathogenesis of neuropathic pain, immunologically based treatment approach will be the critical point of treatment.

산지별(産地別) 봉독액약침자극(峰毒液藥鍼刺戟)이 면역기능저하(免疫機能低下)에 미치는 영향(影響) (The Effect of Honey Bee Venom Aqua-Acupuncture by its Production from Different Regions on Decreased Immune Response)

  • 이경희;김창환;강성길;고형균
    • Journal of Acupuncture Research
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    • 제17권4호
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    • pp.28-40
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    • 2000
  • Objectives : This study was purposed to investigate the effect of honey bee venom aqua-acupuncture on decreased immune response by its production from Korea, North America and China. Methods : ICR-mouse was exposed with four minute sublethal 60Co- $\gamma$ -ray irradiation onto the body and got a series of each country's 0.1 ml honey bee venom aqua-acupuncture to Choksamni(ST36) every other day for three times. Thereafter the numbers of WBC, delayed type hypersensitivity, hemagglutinin titers, hemolysin titers, quantitation of T-cell and B-cell, lymphocyte transformation, natural killer cell activity, interleukin-2 productivity and interferon productivity were measured. Results : The numbers of WBC, delayed type hypersensitivity, hemagglutinin titers, hemolysin titers, quantitation of T-cell and B-cell and lymphocyte transformation were increased respectively with statistical significance in Korean, North American and Chinese honey bee venom aqua-acupuncture groups as compared with the control group. The natural killer cell activity was increased with statistical significance in Korean honey bee venom aqua-acupuncture group, and Interleukin-2 productivity and interferon productivity were not shown any statistical significance in all experimental groups as compared with the control group. Conclusions : According to the results, honey bee venom aqua-acupuncture has significant effect on decreased immune response, and Korean bee venom can be substituted for North American and Chinese one.

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알러지성 비염 병태 모델에 대한 방풍통성산(防風通聖散)의 항알러지 효과 (The Effect of Bangpungtongsung-San on Model of Allergic Rhinitis)

  • 김희정;박외숙;김규석;차재훈;김윤범
    • 한방안이비인후피부과학회지
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    • 제19권1호
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    • pp.21-30
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    • 2006
  • Background and Objective : Allergic rhinitis is a IgE-mediated hypersensitive reaction at nasal mucosa. In oriental medicine, Bangpungtongsung-San is clinically widely used for the treatment of the allergic rhinitis. The objective of this study is to investigate the effects of Bangpungtongsung-San on allergic rhinitis experimentally. Material and Methods : BALB/c mouse were divided into there groups: intact, control, experimental groups. Control and experimental group were induced allergic rhinitis by Ovalbumin as· the method of Levin and Vaz. Experimental group was orally administered the Bangpungtongsung-San for 28days. Total IgE, Interleukin-4, Interleukin-5 and $Interferon-{\gamma}$ were measured at three groups. The statistical significance was examined by Independent Samples T test. Results : 1. The experimental group shows increase of $IFN-{\gamma}$ by 17% compared with control group but there was no statistical significance. 2. The experimental group shows increase of IL-4 and IL-5 compared with control group but there was no statistical significance. 3. The experimental group shows increase of Total IgE and diminution of OVA-specific IgE by 32% compared with control group but there was no statistical significance. Conclusion : The effect of Bangpungtongsung-San on allergic rhinitis is not immunological but seems to be anti-imflammatory and anti-stress effect.

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Effect of saccharin on inflammation in 3T3-L1 adipocytes and the related mechanism

  • Kim, Hye Lin;Ha, Ae Wha;Kim, Woo Kyoung
    • Nutrition Research and Practice
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    • 제14권2호
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    • pp.109-116
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    • 2020
  • BACKGROUND/OBJECTIVES: Excessive intake of simple sugars induces obesity and increases the risk of inflammation. Thus, interest in alternative sweeteners as a sugar substitute is increasing. The purpose of this study was to determine the effect of saccharin on inflammation in 3T3-L1 adipocytes. MATERIALS/METHODS: 3T3-L1 preadipocytes were differentiated into adipocytes. The adipocytes were treated with saccharin (0, 50, 100, and 200 ㎍/mL) for 24 h. Inflammation was induced by exposure of treated adipocytes to lipopolysaccharide (LPS) for 18 h and cell proliferation was measured. The concentration of nitric oxide (NO) was measured by using Griess reagent. Protein expressions of nuclear factor kappa B (NF-κB) and inhibitor κB (IκB) were determined by western blot analysis. The mRNA expressions of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin 1β (IL-1β), interleukin 6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-α (TNF-α) were determined by real-time PCR. RESULTS: Compared with the control group, the amount of NO and the mRNA expression of iNOS in the LPS-treated group were increased by about 17.6% and 46.9%, respectively, (P < 0.05), and those parameter levels were significantly decreased by saccharin treatment (P < 0.05). Protein expression of NF-κB was decreased and that of IκB was increased by saccharin treatment (P < 0.05). Saccharin decreased the mRNA expression of COX-2 and the inflammation cytokines (IL-1β, IL-6, MCP-1, and TNF-α) (P < 0.05). CONCLUSIONS: The results of this study suggest that saccharin can inhibit LPS-induced inflammatory responses in 3T3-L1 adipocytes via the NF-κB pathway.

House Dust Mite Extract Induces $PLC/IP_3$-dependent $Ca^{2+}$ Signaling and IL-8 Expression in Human Gingival Epithelial Cells

  • Son, Ga-Yeon;Son, Aran;Park, Wonse;Shin, Dong Min
    • International Journal of Oral Biology
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    • 제40권1호
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    • pp.11-17
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    • 2015
  • The gingival epithelium of the oral cavity is constantly exposed to exogenous stimuli such as bacterial toxins, allergens, and thermal changes. These exogenous stimuli are resisted by innate host defense in gingival epithelial cells. However, it is unclear exactly how the exogenous stimuli affect detrimentally on the human gingival epithelial cells. Here, we investigated whether the allergen, such as house dust mite (HDM) extract, is linked to $Ca^{2+}$ signaling and proinflammatory cytokine expression in primary cultured human gingival epithelial cells. HDM extract induced an increase in intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) in a dose-dependent manner. Extracellular $Ca^{2+}$ depletion did not affected on the HDM extract-induced increase in $[Ca^{2+}]_i$. The HDM extract-induced increase in $[Ca^{2+}]_i$ was abolished by the treatment with U73122 and 2-APB, which are inhibitors of phospholipase C (PLC) and inositol 1,4,5-trisphosphate ($IP_3$) receptor. Moreover, HDM extract induced the mRNA expression of pro-inflammatory cytokine, interleukin (IL)-8. These results suggest that HDM extract triggers $PLC/IP_3$-dependent $Ca^{2+}$ signaling and IL-8 mRNA expression in primary cultured human gingival epithelial cells.

Persicaria senticosa Ameliorates Imiquimod-induced Psoriasis-like Skin Lesions in Mice via Suppression of IL-6/STAT3 Expression and Proliferation of Keratinocytes

  • Jung, Sangmi;Park, Jeong-Ran;Ra, Moonjin;Kim, Young Han;Yu, Ji Hoon;Lee, Yongjun
    • Natural Product Sciences
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    • 제26권2호
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    • pp.136-143
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    • 2020
  • Psoriasis is one of the most common inflammatory skin disorders, with a global prevalence of 2% - 3%. It is an autoimmune skin disorder characterized by excessive generation of plaques on the skin with typical long-lasting red, itchy, and scaly lesions. In this study, we aimed to elucidate the anti-psoriatic effect of the methanolic extract of Persicaria senticosa (PS), a bioactive edible plant extract used in traditional medicine, using a mouse model of imiquimod (IMQ)-induced psoriasis. The daily topical application of IMQ could induce human psoriasis-like lesion. The extract ameliorated IMQ-induced psoriasis. Furthermore, hematoxylin and eosin staining and the Psoriasis Area and Severity Index (PASI) scores indicated that topical application of PS led to an improvement in erythema, scaling, and thickness scores of the mouse dorsal skin and a considerable decrease in the epidermal thickness of the ear and dorsal skin in the IMQ-induced psoriatic mouse model. We also studied the effect of PS on the proliferation of keratinocytes using HaCaT cells. The extract inhibited cell proliferation and IL-6 and pSTAT3 expression induced by M5 cocktail (comprising interleukin [IL]-1α, IL-17A, IL-22, oncostatin M, and tumor necrosis factor-α) in HaCaT cells. Thus, PS might serve as a potential therapeutic agent for the treatment of psoriasis.

Role of AMP-Activated Protein Kinase (AMPK) in Smoking-Induced Lung Inflammation and Emphysema

  • Lee, Jae Seung;Park, Sun Joo;Cho, You Sook;Huh, Jin Won;Oh, Yeon-Mok;Lee, Sang-Do
    • Tuberculosis and Respiratory Diseases
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    • 제78권1호
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    • pp.8-17
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    • 2015
  • Background: AMP-activated protein kinase (AMPK) not only functions as an intracellular energy sensor and regulator, but is also a general sensor of oxidative stress. Furthermore, there is recent evidence that it participates in limiting acute inflammatory reactions, apoptosis and cellular senescence. Thus, it may oppose the development of chronic obstructive pulmonary disease. Methods: To investigate the role of AMPK in cigarette smoke-induced lung inflammation and emphysema we first compared cigarette smoking and polyinosinic-polycytidylic acid [poly(I:C)]-induced lung inflammation and emphysema in $AMPK{\alpha}1$-deficient ($AMPK{\alpha}1$-HT) mice and wild-type mice of the same genetic background. We then investigated the role of AMPK in the induction of interleukin-8 (IL-8) by cigarette smoke extract (CSE) in A549 cells. Results: Cigarette smoking and poly(I:C)-induced lung inflammation and emphysema were elevated in $AMPK{\alpha}1$-HT compared to wild-type mice. CSE increased AMPK activation in a CSE concentration- and time-dependent manner. 5-Aminoimidazole-4-carboxamide-1-${\beta}$-4-ribofuranoside (AICAR), an AMPK activator, decreased CSE-induced IL-8 production while Compound C, an AMPK inhibitor, increased it, as did pretreatment with an $AMPK{\alpha}1$-specific small interfering RNA. Conclusion: $AMPK{\alpha}1$-deficient mice have increased susceptibility to lung inflammation and emphysema when exposed to cigarette smoke, and AMPK appears to reduce lung inflammation and emphysema by lowering IL-8 production.