• 제목/요약/키워드: Inflammatory Cytokine

검색결과 1,587건 처리시간 0.027초

개에서 DNCB에 의해 유발된 알레르기성 접촉피부염에 대한 아로마 오일 합제의 항염증 효과 (Anti-inflammatory Effects of Aroma Oil Complex on DNCB-Induced Allergic Contact Dermatitis in Dogs)

  • 오동규;오태호
    • 한국임상수의학회지
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    • 제31권3호
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    • pp.180-193
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    • 2014
  • 알러지성 접촉피부염은 T세포와 대식세포가 관여하는 세포매개성 면역반응으로 항원에 노출된 뒤 수 일 후에 증상이 발현되는 지연형 반응으로 특이 T세포의 활성을 통해 다양한 cytokine이 분비되어 항원 유입부위로 염증세포의 유주로 염증이 발생한다. 본 연구에서는 DNCB로 유발한 알러지성 접촉피부염에 대한 아로마 오일 합제의 항염효과를 평가하였다. 아로마 오일 합제는 8일간 적용하였고 실험기간 동안 2일 간격으로 피부 생물리학적 지표를 측정한 후 피부생검을 통해 피부조직을 평가하였다. DNCB 적용 후 피부 생물리학적 지표인 표피경유수분손실, 피부 수화도, 피부 두께 그리고 홍반지수가 증가하였다 (p < 0.05). 피부조직 평가에서 염증세포 침윤과 부종성 변화에 의한 상피두께 증가 및 진피 결합조직의 감소가 특징적으로 나타났다. 또한 진피내 pro-inflammatory cytokine인 TNF-${\alpha}$와 IFN-${\gamma}$ 면역반응세포수 및 표피내 apoptotic change의 지표인 caspase-3와 PARP 면역반응세포의 수가 유의적으로 증가 하였다 (p<0.01). 그러나 아로마 오일 합제 적용후에는 피부 생물리학적 지표 (p<0.05) 및 피부조직의 병리적 변화는 (p<0.01) 기저상태로 회복되었다. 따라서 본 연구를 통해 개에서 DNCB에 의한 알레르기성 접촉피부염 유발 및 아로마 오일 합제의 우수한 항염증 효과를 확인하였고 아로마 오일 합제는 향후 피부염에 대한 치료제로 사용할 수 있을 것으로 기대된다.

Propionibacterium acnes에 의해 유도되는 염증반응에서 Cnestis palala (Lour.) Merr. 추출물의 억제효과 (Cnestis palala (Lour.) Merr. extract suppresses Propionibacterium acnes-induced inflammation)

  • 신진학;이은혜;김선숙;;서수련
    • 미생물학회지
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    • 제54권1호
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    • pp.38-45
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    • 2018
  • 여드름은 사춘기와 젊은 연령층에서 나타나는 염증성 피부질환이다. Propionibacterium acnes (P. acnes)는 여드름에서 염증을 유발하는 주요한 균으로 알려져 있다. P. acnes 는 피부에서 과잉생산된 피지에 의해 막힌 모낭 내에서 증식하며, 피부 내의 단핵구를 활성화시키고 염증성 사이토카인(pro-inflammatory cytokine)의 분비를 촉진하여 염증반응을 증가시키는 것으로 알려져 있다. 본 논문에서는 Cnestis palala (Lour.) Merr. 추출물이 P. acnes 에 의한 염증반응을 감소시킬 수 있는지 확인하고자 하였다. 마우스 대식세포주인 RAW264.7 에서 C. palala 추출물은 P. acnes 에 의해 증가하는 염증성 사이토카인인 $IL-1{\beta}$의 단백질 발현량과 IL-6, $TNF-{\alpha}$, COX-2 의 mRNA 발현량을 감소시켰다. 또한 염증성 사이토카인 발현의 주요 전사인자(transcription factor)인 $NF-{\kappa}B$ 의 전사 활성 역시 C. palala 추출물에 의해 감소하는 것을 확인하였다. 따라서 C. palala 추출물이 P. acnes 에 의해 발생하는 여드름의 치료제나 그 보조제로 사용될 가능성이 있음을 제안 할 수 있다.

레드 비트 뿌리 추출물의 항산화 및 항염증 효과 (Antioxidant and anti-inflammatory activity of extracts from red beet (Beta vulagaris) root)

  • 이미란;강창희;부희정
    • 한국식품저장유통학회지
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    • 제24권3호
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    • pp.413-420
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    • 2017
  • 본 연구는 제주도에서 재배된 레드 비트(B. vulagaris) 뿌리의 항산화 및 항염 효과를 알아보기 위하여 70% EtOH 추출물과 순차적 용매 분획물들을 확보하여 총폴리페놀 함량 및 ABTS 라디칼 소거 활성 측정을 통한 항산화 효능평가와 대식세포인 RAW264.7 세포에 LPS를 자극한 후 iNOS/NO, $COX-2/PGE_2$ 및 전염증성 cytokine을 유도하여 염증 억제 효과를 알아보았다. 그 결과, 총 폴리페놀이 37.02 mg GAE/g로 가장 높게 나온 EtOAc 분획물이 라디칼 소거활성도 가장 우수하게 나타났으며($IC_{50}$ $42.9{\mu}g/mL$), 대조군으로 사용한 BHT($IC_{50}$ $57.4{\mu}g/mL$)보다 좋은 활성을 보였다. 항염 활성 분석을 위하여 NO/iNOS, $PGE_2/COX-2$, 및 염증성 cytokine($TNF-{\alpha}$, IL-6, $IL-1{\beta}$)의 생성 억제 효능을 분석한 결과, 총 폴리페놀 함량 결과와는 유의적이지 않게 hexane 분획물이 처리 농도 범위(50, 100, 200, $300{\mu}g/mL$)에서 NO/iNOS, $PGE_2/COX-2$, 및 염증성 cytokine 생성을 유의적으로 억제하였다. iNOS와 COX-2 단백질 발현 억제 효과를 통해 NO와 $PGE_2$ 생성 억제에 영향을 끼치고 있음을 확인하였고, 염증성 cytokine 중에는 IL-6의 생성을 가장 강하게 억제함으로써 전체적으로 항염 활성에 영향을 미치고 있음을 확인할 수 있었다. 이러한 결과들로부터 레드비트 뿌리의 EtOAc 분획물에서의 항산화 효능 확인과 hexane 분획물의 세포내 항염 효과를 알 수 있었으며, 향후 유효 물질 동정을 통한 기전 연구를 하는 데 대한 기초자료로 활용할 수 있을 것이라 사료된다.

Inhibitory Effect of S100A8 on Neutrophil Apoptosis by Cytokine Release of Normal and Allergic Monocytes

  • Lee, Ji-Sook
    • 대한의생명과학회지
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    • 제26권3호
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    • pp.226-229
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    • 2020
  • S100A8 functions as an essential factor in inflammatory response. Cytokine release of monocytes and regulation of neutrophil apoptosis are important steps in pathogenesis of allergy. This study aims to examine the relation between cytokine release of monocytes due to S100A8 and neutrophil apoptosis. S100A8 enhanced the release of IL-6 and IL-8 in monocytes of normal and allergic subjects. Treatment of supernatants of normal and allergic monocytes with S100A8 blocked neutrophil apoptosis by inhibition of caspase 9 and caspase 3 activation. The secretion signal induced by S100A8 is involved in TLR4, Src family protein, PKCδ, ERK1/2, p38 MAPK, JNK, and NF-κB. These findings may contribute to understanding the complex pathogenesis of allergic diseases by determining inflammatory responses associated with S100A8, monocytes, and neutrophils.

The inhibitory effects of Gami-Phedoc-San on TNF-α, IL-1β and IFN-γ secretion from human monocytes

  • Kim Mi-Sun;Lee Eun-Hee;Choung Se-Young
    • Advances in Traditional Medicine
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    • 제2권1호
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    • pp.41-46
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    • 2002
  • In our study, the several cytokines were determined in phytohaemagglutinin (PHA)-stimulated peripheral blood mononuclear cells (PBMC) of Adamantiades-Behcets patients. Adamantiades-Behcets disease (ABD) is a systemic inflammatory disorder and might involve immune dysfunction. High levels of $TNF-\alpha,\;IL-1\beta$ and $IFN-{\gamma}$ indicate the activation of inflammatory reactions and immune system in ABD. Gami-Phedoc-San (GPS) is an Oriental herbal medication, which has been used in Korea for the treatment of ABD. GPS (1 mg/ ml) significantly inhibited the secretion of proinflammatory cytokines, $TNF-\alpha\;and\;IL-1\beta$, compared to absence of GPS (by $50.5{\pm}1.9%$ inhibition for $TNF-\alpha$ and $106.9{\pm}16.8%$ for $IL-1\beta$). GPS also inhibited the production of $IFN-\gamma$, immunoregulatory Th1 cytokine, by $78.4{\pm}2.8%$. The inhibitory effects of GPS on cytokine secretion showed dose-dependent manner, and the pre-treatment of 1 mg/ml GPS had better effects than immunosuppressive drug for treatment of ABD, cyclosporin A. Our results suggest that GPS treatment for ABD patients might have pharmacological activity of immune and inflammatory responses through the cytokine modulation.

염증성 치은조직과 치주인대세포에서 Cytokine에 의해 유도되는 열충격단백 발현에 관한 연구 (Expression of Heat Shock Protein in Cytokine Stimulated PDL Cells and Inflamed Gingival Tissue)

  • 조인호;김덕규;김은철;유형근;신형식
    • Journal of Periodontal and Implant Science
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    • 제28권1호
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    • pp.103-120
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    • 1998
  • Prokaryotic and eukaryotic cells respond to heat stress and other environmental abuses by synthesizing a small set of stress proteins and by inhibiting post-transcription synthesis of normal proteins. The purpose of the present study was to document the stress response produced by inflamed gingival tissue in vivo, and cytokine inducted human periodontal ligament cells. Human PDL cells were exposed to TNF-$\alpha$(1ng/ml), INF-$\gamma$(200 U/ml), LPS(100ug/ml), combination of cytokine, and SDS-PAGE gels running and Western blotting analysis was done. In vivo studies, the healthy gingival tissusse of a control group and inflamed gingival tissue of adult periodontitis were studied by immunohistochemistry and histology. The results were as follows 1. HSP 47 was distributed on basal layer in healthy gingiva, but stronger stained in basal, suprabasal, and spinous layer of inflamed gingiva. 2. HSP 47 was rare on endothelial cells and mononuclear cells in healthy gingiva, but stronger expressed in inflamed gingiva. 3. HSP 70 expression was rare on epihelium and inflammatory cells hi both healthy & inflamed gingiva. 4. HSP 70 was actively expressed on endothelial cells and inflammatory cells of capillary lumen in moderately & mild inflamend gingiva. 5. PDL cells showed low level of HSP 47 protein expression which was significantly induced by cytokine stimulation (LSP only and combination). 6. Maximum HSP 70 protein induction was seen with stimulation by a combination of the cytokine, Combination of TNF-$\alpha$, INF-$\gamma$, LPS have been shown to synergistically effects of HSP 70 expression. On the above findings, HSP Is influenced by cytokine and chronic inflammation in vivo, and may be involved in protection of tissue during periodontal inflammatiom.

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Proliferation of Mouse Prostate Cancer Cells Inflamed by Trichomonas vaginalis

  • Kim, Sang-Su;Kim, Kyu-Shik;Han, Ik-Hwan;Kim, Yeseul;Bang, Seong Sik;Kim, Jung-Hyun;Kim, Yong-Suk;Choi, Soo-Yeon;Ryu, Jae-Sook
    • Parasites, Hosts and Diseases
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    • 제59권6호
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    • pp.547-556
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    • 2021
  • Our objective was to investigate whether inflammatory microenvironment induced by Trichomonas vaginalis infection can stimulate proliferation of prostate cancer (PCa) cells in vitro and in vivo mouse experiments. The production of CXCL1 and CCL2 increased when cells of the mouse PCa cells (TRAMP-C2 cell line) were infected with live T. vaginalis. T. vaginalis-conditioned medium (TCM) prepared from co-culture of PCa cells and T. vaginalis increased PCa cells migration, proliferation and invasion. The cytokine receptors (CXCR2, CCR2, gp130) were expressed higher on the PCa cells treated with TCM. Pretreatment of PCa cells with antibodies to these cytokine receptors significantly reduced the proliferation, mobility and invasiveness of PCa cells, indicating that TCM has its effect through cytokine-cytokine receptor signaling. In C57BL/6 mice, the prostates injected with T. vaginalis mixed PCa cells were larger than those injected with PCa cells alone after 4 weeks. Expression of epithelial-mesenchymal transition markers and cyclin D1 in the prostate tissue injected with T. vaginalis mixed PCa cells increased than those of PCa cells alone. Collectively, it was suggested that inflammatory reactions by T. vaginalis-stimulated PCa cells increase the proliferation and invasion of PCa cells through cytokine-cytokine receptor signaling pathways.

The role of interleukin-17 in bone metabolism and inflammatory skeletal diseases

  • Lee, Youngkyun
    • BMB Reports
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    • 제46권10호
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    • pp.479-483
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    • 2013
  • The balance between osteoblast-dependent bone formation and osteoclast-dependent bone resorption maintains bone homeostasis. In inflammatory conditions, this balance shifts toward bone resorption, causing osteolytic bone lesions observed in rheumatoid arthritis and periodontitis. A recently discovered family of cytokine IL-17 is widely reported to mediate diverse inflammatory processes. During the last decade, novel roles for IL-17 in skeletal homeostasis have been discovered indicating the potential importance of this cytokine in bone metabolism. This review will summarize and discuss the involvement of IL-17 during bone homeostasis in both physiologic and pathologic conditions. A better understanding of the role of IL-17 in skeletal systems warrants an advance in bone biology, as well as development of therapeutic strategies against bone-lytic diseases, such as rheumatoid arthritis and periodontitis.

Autophagy down-regulates NLRP3-dependent inflammatory response of intestinal epithelial cells under nutrient deprivation

  • Yun, Yewon;Baek, Ahruem;Kim, Dong-Eun
    • BMB Reports
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    • 제54권5호
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    • pp.260-265
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    • 2021
  • Dysregulation of inflammation induced by noninfectious stress conditions, such as nutrient deprivation, causes tissue damage and intestinal permeability, resulting in the development of inflammatory bowel diseases. We studied the effect of autophagy on cytokine secretion related to intestinal permeability under nutrient deprivation. Autophagy removes NLRP3 inflammasomes via ubiquitin-mediated degradation under starvation. When autophagy was inhibited, starvation-induced NLRP3 inflammasomes and their product, IL-1β, were significantly enhanced. A prolonged nutrient deprivation resulted in an increased epithelial mesenchymal transition (EMT), leading to intestinal permeability. Under nutrient deprivation, IL-17E/25, which is secreted by IL-1β, demolished the intestinal epithelial barrier. Our results suggest that an upregulation of autophagy maintains the intestinal barrier by suppressing the activation of NLRP3 inflammasomes and the release of their products, including pro-inflammatory cytokines IL-1β and IL-17E/25, under nutrient deprivation.