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      Cooperative effect of Alternaria and rhinovirus on the activation of nasal polyp epithelial cells

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      https://www.riss.kr/link?id=A103912316

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      다국어 초록 (Multilingual Abstract)

      Background and Objectives : The nasal epithelium is the first barrier encountered by airborne allergens and is an active participant in airway inflammation. The aim of this study was to determine the activation mechanism of nasal epithelial cells with Alternaria and the effect of rhinovirus on the Alternaria induced activation of nasal epithelial cells. Materials and methods : Cultured epithelial cells were stimulated by Alternaria with or without rhinovirus-16 (RV-16) infection. Release of interleukin (IL)-6, IL-8, and granulocyte macrophage colony-stimulating factor (GM-CSF) into culture supernatants were measured to determine the activation of epithelial cells. Nuclear factor-κB (NF-κB) and activator protein-1 (AP-1) of the epithelial cells were analyzed using western blot analysis. Intracellular NF-kB and AP-1 activity were evaluated by enzyme-linked immunosorbent assay. To determine the epithelial cell activation mechanism, cytokine production was inhibited with NF-kB, AP-1, and mitogen activated protein kinase (MAPK) inhibitors. Results : Exposure of epithelial cells to Alternaria enhanced the production of cytokines. Intracellular NF-kB expression and activity were significantly increased by Alternaria, but not by RV-16. AP-1 expression and activity were not influenced by Alternaria. Increased IL-6 production was significantly inhibited by transcription factor inhibitors. However, IL-8 and GM-CSF production were not inhibited by these transcription factor inhibitors. Conclusions : Our in-vitro results demonstrate that Alternaria activates nasal polyp epithelial cells via NF-kB pathway and that NF-kB, AP-1, and MAPK are involved in the production of IL-6.
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      Background and Objectives : The nasal epithelium is the first barrier encountered by airborne allergens and is an active participant in airway inflammation. The aim of this study was to determine the activation mechanism of nasal epithelial cells with...

      Background and Objectives : The nasal epithelium is the first barrier encountered by airborne allergens and is an active participant in airway inflammation. The aim of this study was to determine the activation mechanism of nasal epithelial cells with Alternaria and the effect of rhinovirus on the Alternaria induced activation of nasal epithelial cells. Materials and methods : Cultured epithelial cells were stimulated by Alternaria with or without rhinovirus-16 (RV-16) infection. Release of interleukin (IL)-6, IL-8, and granulocyte macrophage colony-stimulating factor (GM-CSF) into culture supernatants were measured to determine the activation of epithelial cells. Nuclear factor-κB (NF-κB) and activator protein-1 (AP-1) of the epithelial cells were analyzed using western blot analysis. Intracellular NF-kB and AP-1 activity were evaluated by enzyme-linked immunosorbent assay. To determine the epithelial cell activation mechanism, cytokine production was inhibited with NF-kB, AP-1, and mitogen activated protein kinase (MAPK) inhibitors. Results : Exposure of epithelial cells to Alternaria enhanced the production of cytokines. Intracellular NF-kB expression and activity were significantly increased by Alternaria, but not by RV-16. AP-1 expression and activity were not influenced by Alternaria. Increased IL-6 production was significantly inhibited by transcription factor inhibitors. However, IL-8 and GM-CSF production were not inhibited by these transcription factor inhibitors. Conclusions : Our in-vitro results demonstrate that Alternaria activates nasal polyp epithelial cells via NF-kB pathway and that NF-kB, AP-1, and MAPK are involved in the production of IL-6.

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      참고문헌 (Reference)

      1 Ponikau JU, "The diagnosis and incidence of allergic fungal sinusitis" 74 : 877-884, 1999

      2 Murray CS, "Study of modifiable risk factors for asthma exacerbation: virus infection and allergen exposure increase the risk of asthma hospital admission in children" 61 : 376-382, 2006

      3 Puhakka T, "Sinusitis in the common cold" 102 : 403-408, 1998

      4 Terajima M, "Rhinovirus infection of primary cultures of human tracheal epithelium: role of ICAM-1 and IL-1beta" 273 (273): L749-L759, 1997

      5 Nicholson KG, "Respiratory viruses and exacerbations of asthma in adults" 307 : 982-986, 1993

      6 Papi A, "Respiratory epithelial cell expression of vascular cell adhesion molecule-1 and its up-regulation by rhinovirus infection via NF-κB and GATA transcription factors" 274 : 30041-30051, 1999

      7 Gern JE, "Relationship of upper and lower airway cytokines to outcome of experimental rhinovirus infection" 162 : 2226-2231, 2000

      8 Shin SH, "Protease-dependent activation of nasal polyp epithelial cells by airborne fungi leads to migration of eosinophils and neutrophils" TAYLOR & FRANCIS AS 126 : 1286-1294, 2006

      9 Kauffman HF, "Protease-dependent activation of epithelial cells by fungal allergens leads to morphologic changes and cytokine production" 105 : 1185-1193, 2000

      10 Rudack C, "PAR-2 activation regulates IL-8 and GRO-α synthesis by NF- κB, but not RANTES, IL-6, eotaxin or TARC expression in nasal epithelium" 37 : 1009-1022, 2007

      1 Ponikau JU, "The diagnosis and incidence of allergic fungal sinusitis" 74 : 877-884, 1999

      2 Murray CS, "Study of modifiable risk factors for asthma exacerbation: virus infection and allergen exposure increase the risk of asthma hospital admission in children" 61 : 376-382, 2006

      3 Puhakka T, "Sinusitis in the common cold" 102 : 403-408, 1998

      4 Terajima M, "Rhinovirus infection of primary cultures of human tracheal epithelium: role of ICAM-1 and IL-1beta" 273 (273): L749-L759, 1997

      5 Nicholson KG, "Respiratory viruses and exacerbations of asthma in adults" 307 : 982-986, 1993

      6 Papi A, "Respiratory epithelial cell expression of vascular cell adhesion molecule-1 and its up-regulation by rhinovirus infection via NF-κB and GATA transcription factors" 274 : 30041-30051, 1999

      7 Gern JE, "Relationship of upper and lower airway cytokines to outcome of experimental rhinovirus infection" 162 : 2226-2231, 2000

      8 Shin SH, "Protease-dependent activation of nasal polyp epithelial cells by airborne fungi leads to migration of eosinophils and neutrophils" TAYLOR & FRANCIS AS 126 : 1286-1294, 2006

      9 Kauffman HF, "Protease-dependent activation of epithelial cells by fungal allergens leads to morphologic changes and cytokine production" 105 : 1185-1193, 2000

      10 Rudack C, "PAR-2 activation regulates IL-8 and GRO-α synthesis by NF- κB, but not RANTES, IL-6, eotaxin or TARC expression in nasal epithelium" 37 : 1009-1022, 2007

      11 Fujioka S, "NF-κB and AP-1 connection: mechanism of NF-κB-dependent regulation of AP-1 activity" 24 : 7806-7819, 2004

      12 Jonhston SL, "Low grade rhinovirus infection induces a prolonged release of IL-8 in pulmonary epithelium" 160 : 6172-6181, 1998

      13 Jang YJ, "Levocetrizine inhibits rhinovirus-induced ICAM-1 and cytokine expression and viral replication in airway epithelialc cells" 81 : 226-233, 2009

      14 Wang CB, "Induction of IL-6 in co-culture of bronchial epithelial cells and eosinophils is regulated by p38 MAPK and NF-κB" 60 : 1378-1385, 2005

      15 Wong CK, "House dust mite allergen Der P1 elevate the release of inflammatory cytokines and expression of adhesion molecules in co-culture of human eosinophils and bronchial epithelial cells" 18 : 1327-1335, 2006

      16 Shin SH, "Fungus culture of the nasal secretion of chronic rhinosinusitis patients: Seasonal variation in Daegu, Korea" 21 : 556-559, 2007

      17 Khalaf H, "Differential cytokine regulation by NF-κB and AP-1 in Jurkat T-cells" 11 : 26-, 2010

      18 Jang YJ, "Detection of rhinovirus in turbinate epithelial cells of chronic sinusitis" 20 : 553-560, 2006

      19 Mullol J, "Cytokine gene expression and release from epithelial cells. A comparision study between healthy nasal mucosa and nasal polyps" 25 : 607-615, 1995

      20 Xaubet A, "Comparison of the role of nasal polyp and normal nasal mucosal epithelial cells on in vitro eosinophil survival. Mediation by GM-CSF and inhibition by dexamethasone" 24 : 307-317, 1994

      21 Kobayashi T, "Asthma-related environmental fungus, Alternaria, activates dendritic cells and produces potent Th2 adjuvant activity" 182 : 2502-2510, 2009

      22 Igarashin Y, "Analysis of nasal secretions during experimental rhinovirus upper respiratory infections" 92 : 722-731, 1993

      23 Bush RK, "Alternaria-induced asthma" 113 : 227-234, 2004

      24 Shin SH, "Airborne fungi induce nasal polyp epithelial cell activation and toll-like receptor expression" 153 : 46-52, 2010

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      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.1 0.1 0.12
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.11 0.11 0.369 0
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