• 제목/요약/키워드: IL-$1{\beta}$ & TNF-${\alpha}$

검색결과 1,238건 처리시간 0.04초

미세분진이 흰쥐의 폐포대식세포에서 TNF-α와 IL-1β의 형성에 미치는 효과 (The Effects of Air-borne Particulate Matters on the Alveolar Macrophages for the TNF-α and IL-1β Secretion)

  • 리천주;이수진;박세종;장병준;이종환;김길수;이명헌;최농훈
    • Tuberculosis and Respiratory Diseases
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    • 제60권5호
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    • pp.554-563
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    • 2006
  • 연구 배경: 대도시의 대기오염은 점차 악화되어 시민의 건강을 위협하고, 심 폐 질환의 발병률과 이 로 인한 사망률을 증가시키고 있다. 서울시 도로가의 PM이 $TNF-{\alpha}$$IL-1{\beta}$의 생성에 직접적으로 어떠한 영향을 미치는지와 PM의 노출이 LPS의 $TNF-{\alpha}$$IL-1{\beta}$의 생성효과에는 어떠한 영향을 미치는지를 평가하고자 하였다. 방 법: 폐렴이 있는 흰쥐와 SPF 흰쥐의 폐포대식세포 각각에 PM을 농도별로 처리하여 분비되는 $TNF-{\alpha}$$IL-1{\beta}$의 농도를 측정하였다. 측정 방법으로는 western blot, ELISA 및 세포면역화학염색법을 이용하였다. 또한 동일 PM 농도에서 배양시간을 달리하여 위와 같이 측정하였다. 결 과: SPF인 흰쥐에서 분리된 페포대식세포에 PM을 단독으로 투여하였을 때 대조군에 비해서 $TNF-{\alpha}$$IL-1{\beta}$의 생성도가 모든 투여군에서 유의하게 증가하였으나, 투여용량의 증가에 따른 유의성은 없었다. 그러나 염증성인 쥐에서 분리된 폐포대식세포에서는 모든 투여군에서 대조군에 비하여 통계학적으로 유의하게 증가하였으며, PM 투여농도의 증가에 따른 생성량도 유의하게 증가하였다. 결 론: PM을 장기간 혹은 일정 농도 이상으로 흡입할 경우 폐포대식세포의 $TNF-{\alpha}$$IL-1{\beta}$의 분비에 영향을 미쳐 새로운 폐질환을 유발할 수 있다. 그러므로 기존에 염증성 폐질환이나 기관지천식이 있는 환자가 미세먼지를 흡입할 경우에는 $TNF-{\alpha}$$IL-1{\beta}$의 생성에 커다란 영향을 미쳐 호흡기 질환을 더욱 악화시킬 가능성이 있을 것으로 추정된다.

Differential Modulatory Effects of Cholera Toxin and Pertussis Toxin on Pain Behavior Induced by TNF-${\alpha}$, Interleukin-1${\beta}$ and Interferon-${\gamma}$ Injected Intrathecally

  • Kwon, Min-Soo;Shim, Eon-Jeong;Seo, Young-Jun;Choi, Seong-Soo;Lee, Jin-Young;Lee, Han-Kyu;Suh, Hong-Won
    • Archives of Pharmacal Research
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    • 제28권5호
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    • pp.582-586
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    • 2005
  • The present study was designed to characterize the possible roles of spinally located cholera toxin (CTX)- and pertussis toxin (PTX)-sensitive G-proteins in pro- inflammatory cy tokine induced pain behaviors. Intrathecal injection of tumor necrosis factor-a (TNF-${\alpha}$; 100 pg), interleukin-1${\beta}$ (IL-1${\beta}$ 100 pg) and interferon-${\gamma}$ (INF-${\gamma}$; 100 pg) showed pain behavior. Intrathecal pretreatment with CTX (0.05, 0.1 and 0.5 mg) attenuated pain behavior induced by TNF-${\alpha}$ and INF-${\gamma}$ administered intrathecally. But intrathecal pretreatment with CTX (0.05, 0.1 and 0.5${\mu}g$) did not attenuate pain behavior induced by IL-1${\beta}$. On the other hand, intrathecal pretreatment with PTX further increased the pain behavior induced by TNF-${\alpha}$ and IL-1${\beta}$ administered intrathecally, especially at the dose of 0.5 ${\mu}g$. But intrathecal pretreatment with PTX did not affect pain behavior induced by INF-${\gamma}$. Our results suggest that, at the spinal cord level, CTX- and PTX-sensitive G-proteins appear to play important roles in modulating pain behavior induced by pro-inflammatory cytokines administered spinally. Furthermore, TNF-${\alpha}$, IL-1${\beta}$ arid INF-${\gamma}$ administered spinally appear to produce pain behavior by different mechanisms.

Nuclear Factor-${\kappa}B$ Dependent Induction of TNF-${\alpha}$ and IL-$1{\beta}$ by the Aggregatibacter actinomycetemcomitans Lipopolysaccharide in RAW 264.7 Cells

  • Na, Hee Sam;Jeong, So Yeon;Park, Mi Hee;Kim, Seyeon;Chung, Jin
    • International Journal of Oral Biology
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    • 제39권1호
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    • pp.15-22
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    • 2014
  • Aggregatibacter actinomycetemcomitans is an important pathogen in the development of localized aggressive periodontitis. Lipopolysaccharide (LPS) is a virulent factor of periodontal pathogens that contributes to alveolar bone loss and connective tissue degradation in periodontal disease. Our present study was designed to investigate the cytokine expression and signaling pathways regulated by A. actinomycetemcomitans LPS (Aa LPS). Cytokine gene expression profiling in RAW 264.7 cells was performed by microarray analyses. The cytokine mRNA and protein levels and related signaling pathways induced by Aa LPS were measured by RT-PCR, ELISA and western blotting. Microarray results showed that Aa LPS strongly induced the expression of NF-${\kappa}B$, NF-${\kappa}B$-related genes, inflammatory cytokines, TNF-${\alpha}$ and IL-$1{\beta}$ in RAW 264.7 cells. NF-${\kappa}B$ inhibitor pretreatment significantly reduced the levels of TNF-${\alpha}$ and IL-$1{\beta}$ mRNA and protein. In addition, the Aa LPS-induced TNF-${\alpha}$ and IL-$1{\beta}$ expression was inhibited by p38/JNK MAP kinase inhibitor pretreatment. These results show that Aa LPS stimulates TNF-${\alpha}$ and IL-$1{\beta}$ expression through NF-${\kappa}B$ and p38/JNK activation in RAW 264.7 cells, suggesting the essential role of this pathway in the pathogenesis of localized aggressive periodontitis.

Canine juvenile cellulitis의 분자생물학적 검사 (Biomolecular Examination of Canine Juvenile Cellulitis)

  • 홍지현;전진;장동우;이완규;양만표;모인필;나기정
    • 한국임상수의학회지
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    • 제20권4호
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    • pp.478-481
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    • 2003
  • Canine juvenile cellulitis (CJC) is a well-recognized lymphocutaneous disease that is seen in young dogs. CJC seemed to be immunologic disorder and may have a hereditary aspect. Exact pathogenesis and cytokine regulation on the immune system of CJC are not clear. CJC was diagnosed in two puppies hospitalized in Veterinary Teaching Hospital of Chungbuk National University. To investigate the cytokine regulation on CJC, RT-PCR was performed with CJC affected dogs. RT-PCR 1 was performed with whole blood sample (CJC-B) and fine needle aspirates of the inguinal lymph node (CJC-LN) from case 1-dog, which included $TNF-\alpha,$ $IL-1\beta,$ $IFN-\gamma,$ IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12 and $\beta-actin.$ Blood sample from a normal dog (N-B) served for a negative control of RT-PCR 1 (case 1). $IFN-\gamma,$ IL-2, IL-4, IL-5, IL-8, IL-10 and IL-12 transcripts were not expressed in all sample. $TNF-\alpha$ and $IL-1\beta,$ were not transcripted from CJC-B but from CJC-LN. On RT-PCR 2 (case 2), submandibular lymph node aspirates were used and $TNF-\alpha,$ IL-10, $IFN-\gamma$ and $IL-1\beta$ were expressed. $TNF-\alpha,$ 1L-10 and $IFN-\gamma$ were secreted from activated macrophages enhance the inflammation in tissue. These results imply that abnormally increased macrophages secret $TNF-\alpha$ and $IL-1\beta$ in the affected lymph nodes, which attract neutrophils and cause inflammation in CJC.

성심지황탕(醒心地黃湯) 열수추출물과 초미세분말제형이 Alzheimer's Disease 병태 모델에 미치는 영향 (Effects of Sungsimjihwang-tang Hot Water Extract & Ultra-fine Powder on the Alzheimer's Disease Model)

  • 민경직;이상룡;정인철
    • 동의생리병리학회지
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    • 제22권5호
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    • pp.1178-1191
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    • 2008
  • This experiment was designed to investigate the effect of the SSJHT hot water extract & ultra-fine Powder on Alzheimer's Disease Model Induced by ${\beta}A$. The effects of the SSJHT hot water extract on expression of IL-1RA, $IL-1{\beta}$$, IL-6, IL-10, $TNF-{\alpha}$, NOS-II, COX-2 mRNA and production of $IL-1{\beta}$, IL-6, $TNF-{\alpha}$ in BV2 microglial cell line treated by lipopolysacchaide(LPS). The effects of the SSJHT hot water extract & ultra-fine powder on (1) the behavior (2) expression of $IL-1{\beta}$, $TNF-{\alpha}$, MDA, CD68, CD11b and AChE (3) and the infarction area of the hippocampus in Alzheimer's diseased mice induced with ${\beta}A$ were investigated. The SSJHT hot water extract suppressed the expression of $IL-1{\beta}$, IL-6 and $TNF-{\alpha}$, NOS-II, COX-2 mRNA and increased IL-1RA, IL-10 in BV2 microglia cell line treated with LPS. The SSJHT hot water extract suppressed the production of $IL-1{\beta}$, IL-6, $TNF-{\alpha}$ significantly in BV2 microglial cell line treated with LPS. The SSJHT hot water extract & ultra-fine powder a significant inhibitory effect on the memory deficit was shown for the mice with Alzheimer's disease induced by ${\beta}A$ in the Morris water maze experiment, which measured step-through latency. The SSJHT hot water extract & ultra-fine powder suppressed the expression of $TNF-{\alpha}$$, $L-1{\beta}$ protein significantly in the microglial cell of mice with Alzheimer's disease induced by ${\beta}A$. The SSJHT hot water extract & ultra-fine powder reduced the MDA and suppressed the over-expression of CD68, CD11b in the mice with Alzheimer's disease induced by ${\beta}A$. The SSJHT hot water extract & ultra-fine powder significantly decreased AChE activity in the serum of the mice with Alzheimer's disease induced by ${\beta}A$. The SSJHT hot water extract & ultra-fine powder reduced infarction area of hippocampus. and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by ${\beta}A$. The results suggest that the SSJHT hot water extract & ultra-fine powder may be effective for treatment of Alzheimer's disease. Investigation into the clinical use of the SSJHT hot water extract & ultra-fine powder for Alzheimer's disease is suggested for future research.

Effects of Omega-3-Rich Harp Seal Oil on the Production of Pro-Inflammatory Cytokines in Mouse Peritoneal Macrophages

  • Choi, Myungwon;Ju, Jaehyun;Suh, Jae Soo;Park, Kun-Young;Kim, Kwang Hyuk
    • Preventive Nutrition and Food Science
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    • 제20권2호
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    • pp.83-87
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    • 2015
  • Omega-3, a polyunsaturated fatty acid, is an essential fatty acid necessary for human health, and it protects against cardiovascular disease, inflammation, autoimmune diseases, and cancer. In the present study, we investigated the effects of omega-3-rich harp seal oil (HSO) on the production of nitric oxide (NO) and cytokines, such as tumor necrosis factor (TNF)-${\alpha}$, interleukin-(IL)-$1{\beta}$, IL-6, and IL-12/IL-23 (p40) in peritoneal macrophages of mice. The culture supernatants of murine macrophages exposed to lipopolysaccharide (LPS), HSO, or HSO+LPS were harvested to assay IL-$1{\beta}$, TNF-${\alpha}$, IL-6, and IL-12/IL-23 (p40) cytokines and NO. TNF-${\alpha}$, IL-$1{\beta}$, and IL-12/IL-23 (p40) levels, except IL-6, were lower in the culture supernatants of mouse peritoneal macrophages exposed to LPS plus HSO than those of the groups exposed to LPS alone. These observations demonstrate that omega-3-rich harp seal oil downregulates the production of the pro-inflammatory cytokines such as IL-$1{\beta}$, TNF-${\alpha}$, and IL-12/IL-23 (p40). These results suggest that HSO could be potentially used as a preventive agent or as an adjunct in anti-inflammatory therapy, if more research results were accumulated.

호염구세포주와 복강 비만세포에서 유색미 겨 추출물의 알레르기 염증 억제활성 (Inhibitory Activity of Pigmented Rice Bran Extract to the Allergic Inflammation in Basophilic Cell Line and Peritoneal Mast Cells)

  • 최선필;강미영;남석현
    • Applied Biological Chemistry
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    • 제48권4호
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    • pp.315-321
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    • 2005
  • 유색미 겨 추출물이 염증반응에 미치는 효과를 호중구 세포주 및 비만세포가 분비하는 염증매개물질인 histamine과 ${\beta}-hexosaminidase$의 분비 및 염증 cytokine 생성에 대한 억제활성을 측정하여 평가하였다. 호중구 세포주인 RBL-2H3 세포와 rat에서 분리 추출한 복강 비만세포(RPMC, peritoneal mast cell)를 이용하여 histamine과 ${\beta}-hexosaminidase$ 분비에 대한 억제활성을 조사한 결과, 일반미 겨 추출물은 RBL-2H3 세포에서 염증매개물질들의 분비량을 증가시킨 반면, 유색미 겨 추출물은 이들의 분비를 억제하였다(histamine 10.19% 억제, ${\beta}-hexosaminidase$ 110.03% 억제). RPMC에서는 유색미가 histamine과 ${\beta}-hexosaminidase$의 분비를 일반미보다 각각 8배와 3배나 높게 억제하는 것으로 나타났다. 염증관련 cytokine으로서 $IL-1{\beta},\;TNF-{\alpha}$ 및 IL-6의 발현을 RT-PCR로 측정한 결과, 유색미가 일반미 보다 $TNF-{\alpha},\;IL-1{\beta}$ 및 IL-6의 발현을 억제하는 효과가 우수하였다. ELISA를 이용하여 cytokine의 분비량을 측정한 실험에서도 유색미가 일반미보다 $TNF-{\alpha},\;IL-1{\beta}$ 및 IL-6의 분비를 효과적으로 억제하였다. 이상의 결과는 유색미가 염증반응의 원인 물질인 histamine과 ${\beta}-hexosaminidase$의 분비에 대한 억제효과 뿐 아니라, 염증 cytokine의 발현을 저해하는 효과도 일반미보다 우수하다는 사실을 보여주었다.

소엽(蘇葉) 추출물이 뇌허혈이 유발된 백서의 cytokine분비에 미치는 영향 (Effects of Folium Perillae on cytokine productions in ischemic rats)

  • 양기호;김형우;조수진;김상대;윤관희;김부여;정현우;조수인
    • 대한본초학회지
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    • 제22권3호
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    • pp.93-99
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    • 2007
  • Objective : The present study was carried out to investigate the effects of Folium Perillae (FP) on several cytokine production such as IL-1$\beta$, TNF-$\alpha$, IL-10 and TGF-$\beta$ to determine related mechanisma in Rats. Methods: So, we investigated the effects of FP on levels of several cytokines such as IL-l$\beta$, TNF-$\alpha$, IL-10 and TGF-$\beta$ in ischemic rats. Results: In this experiment, IL-10, an immune-modulatory cytckine, level was elevated by treatment with FP, but another regulatory cytokine, TGF-$\beta$1 level was not affected. On the other hand, levels of IL-l$\beta$ and TNF-$\alpha$, an inflammatory cytokines, were lowered by treatment with FP effectively. Conclusion : In conclusion, these results suggest that FP is useful to treat patient with disease related to cerebral ischemia, because FP can elevate IL-10 level, lower IL-l$\beta$ and TNF-$\alpha$ levels.

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율무 추출물의 마우스 비장세포와 대식세포 활성 효과 (Effects of Job's Tears(Yul-Moo) Extracts on Mouse Splenocyte and Macrophage Cell Activation)

  • 류혜숙
    • 한국식품영양학회지
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    • 제21권1호
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    • pp.1-6
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    • 2008
  • Job's Tears(Yul-Moo) is a grass crop long-used as a traditional medicine; it is also a nourishing food. There are reports of its anti-inflammatory, stomachic, antiallergic activity, and antispastic effects and Job's Tears has been used in China to treat rheumatism, and neuralgia although its warts, rheumanism remains unclear. Thus, the present study was performed to investigate the in vitro effect of Job's Tears extracts on immune function. Here mouse splenocyte proliferation and cytokine production$(IL-1{\beta},\;IL-6,\;TNF-{\alpha})$ by peritoneal macrophages cultured with ethanol and water extracts of Job's Tears were examined. splenocytes proliferation increased with Job's Tears water extracts supplement at concentrations investigated The cytokine production$(IL-1{\beta},\;IL-6,\;TNF-{\alpha})$ by ELISA using a cytokine kit And $IL-1{\beta}$, IL-6 and $TNF-{\alpha}$ production increased water extracts supplementation. This in vitro study suggests that supplementation with Job's Tears water extracts may enhance immune function by regulating the splenocyte proliferation and enhancing cytokine production of activated macrophages.

Baicalein이 Lipopolysaccharide에 의한 생쥐의 Neuroinflammation에 미치는 영향 (Effects of Baicalein on Neuroinflammation in Lipopolysaccharide-treated Mice)

  • 하경운;김연섭
    • 대한본초학회지
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    • 제28권2호
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    • pp.93-101
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    • 2013
  • Objects : Baicalein is a major bioactive flavonoid component of Scutellaria baicalensis Georgi that shows a wide range of biological activities, including neuroprotections and anti-inflammatory actions. Hence it is a potential therapeutic material for the treatment of neuroinflammation. In this study, we investigated the modulatory effect of baicalein on neuroinflammation. Method : Pro-inflammatory cytokines (TNF-${\alpha}$, IL-$1{\beta}$ and IL-6 mRNA), COX-2 mRNA expression and microglial activation in the brain tissue is induced by systemic lipopolysaccharide (LPS) treatment in C57BL/6 mice. Baicalein was treated orally with 10, 20, and 30 mg/kg 1 hour prior to the LPS (3 mg/kg, i.p.) injection. TNF-${\alpha}$, IL-$1{\beta}$, IL-6 and COX-2 mRNA expression in the brain tissue was measured by the quantitative real-time polymerase chain reaction(PCR) method. Iba1 expression in the brain was measured by western blotting method. Microglia was observed with immunohistochemistry. Results : Baicalein 30 mg/kg significantly attenuated the expression of TNF-${\alpha}$, IL-$1{\beta}$, IL-6 and COX-2 mRNA in the brain tissue. Baicalein 20 mg/kg significantly attenuated the expression of IL-6 mRNA in the brain tissue. Baicalein 30 mg/kg significantly attenuated the expression of Iba1 protein expression in the brain tissue. Baicalein 30 mg/kg significantly decreased the number and cell size of microglia in the cerebral cortex and hypothalamic region and the area percentage of Iba1-expressed microglia in the hippocampus. Conclusion : These results demonstrated that baicalein attenuates LPS induced neuroinflammation in the mice via reduction of pro-inflammatory cytokines (TNF-${\alpha}$, IL-$1{\beta}$, IL-6), COX-2 mRNA expression and microglial activation.