• Title/Summary/Keyword: macophage

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Immune-stimulating Effects of Polygonum aviculare L. Extract on Macrophages (마디풀(Polygonum aviculare L.) 추출물의 대식구 면역증강 효과)

  • Jeon, Chang Bae;Kim, Young Hoon;Batsuren, Dulamjav;Tunsag, Jigjidsuren;Nho, Chu Won;Pan, Cheol-Ho;Lee, Jae Kwon
    • YAKHAK HOEJI
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    • v.57 no.6
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    • pp.394-399
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    • 2013
  • In this study we demonstrated whether the extract of Polygonum aviculare L. (PAE) can be applied to the immune-stimulating responses in macrophages (Raw 264.7 cells). Cell viability was determined by WST-8 assay, and all four doses of PAE (5, 10, 20, and 40 ${\mu}g/ml$) had no significant cytotoxicity during the entire experimental period. PAE increased the production of inducible nitric oxide synthase (iNOS) and nitric oxide (NO), and mRNA expressions and protein levels of pro-inflammatory cytokines(tumor necrotic factor (TNF)-${\alpha}$, interleukin (IL)-$1{\beta}$ and IL-6) in the same cells. These immune-stimulating activities of PAE were found to be caused by the stimulation of $NF{\kappa}B$ signal and phosphorylation of MAP kinases (p38, ERK and JNK).

Effects of Pseudomonas fluorescens on Production of Several Inflammatory Mediators in the Human Alveolar Epithelial Cells. (재조합 단백질 생산에 이용되는 Pseudomonas fluorescens의 인체 폐포 상피세포의 염증성 인자들의 발현에 미치는 영향)

  • Yang, Hyun;Ryoo, Jung-Min;Park, Seung-Hwan;Choi, Hye-Jin;Kim, Na-Yeon;Cho, Hyung-Hoon;Ahn, Jung-Hoon;Moon, Yu-Seok
    • Journal of Life Science
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    • v.18 no.4
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    • pp.530-536
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    • 2008
  • To investigate the molecular mechanism of the airway inflammation by Pseudomonas fluorescens, effects on the inflammatory mediators such as interleukin-8 (IL-8), cyclooxygenase-2 (COX-2), macophage inhibitory cytokine 1 (MIC-1) were assessed in the human alveolar epithelial cells. Exposure to P. fluorescens and its recombinant bacteria suppressed cellular viability in the A549 epithelial cells and pro-inflammatory cytokine interleukin-8 production. However, pro-inflammatory prostaglandin-producing COX-2 protein was not altered by P. fluorescens though its mRNA was slightly elevated. As the inhibitory cytokine for the pro-inflammatory mediators, MIC-1 expression was monitored in A549 cells. MIC-1 gene induction was not significantly enhanced but the protein processing was changed by exposure to P. fluorescens. Pro-protein form of MIC-1 (${\sim}40\;kD$) was cleaved into active form mature MIC-1 (${\sim}15\;kD$) and propeptide (${\sim}28\;kD$) by the bacteria exposure. MIC-1 activation can contribute to the suppression of cellular viability by P. fluorescens and can retard IL-8-induced monocyte recruitment. However, sustained activation of MIC-1 can mediate the tissue injury by P. fluorescens exposure.