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      KCI등재 SCOPUS SCIE

      Acetyl salicylic acid inhibits Th17 airway inflammation via blockade of IL-6 and IL-17 positive feedback

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      https://www.riss.kr/link?id=A101634897

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      다국어 초록 (Multilingual Abstract)

      T-helper (Th)17 cell responses are important for the development of neutrophilic inflammatory disease. Recently, we found that acetyl salicylic acid (ASA) inhibited Th17 airway inflammation in an asthma mouse model induced by sensitization with lipopo...

      T-helper (Th)17 cell responses are important for the development of neutrophilic inflammatory disease. Recently, we found that acetyl salicylic acid (ASA) inhibited Th17 airway inflammation in an asthma mouse model induced by sensitization with lipopolysaccharide (LPS)-containing allergens. To investigate the mechanism(s) of the inhibitory effect of ASA on the development of Th17 airway inflammation, a neutrophilic asthma mouse model was generated by intranasal sensitization with LPS plus ovalbumin (OVA) and then challenged with OVA alone. Immunologic parameters and airway inflammation were evaluated 6 and 48 h after the last OVA challenge. ASA inhibited the production of interleukin (IL)-17 from lung T cells as well as in vitro Th17 polarization induced by IL-6. Additionally, ASA, but not salicylic acid, suppressed Th17 airway inflammation,which was associated with decreased expression of acetyl-STAT3 (downstream signaling of IL-6) in the lung. Moreover, the production of IL-6 from inflammatory cells, induced by IL-17, was abolished by treatment with ASA, whereas that induced by LPS was not. Altogether, ASA, likely via its acetyl moiety, inhibits Th17 airway inflammation by blockade of IL-6 and IL-17positive feedback.

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      참고문헌 (Reference)

      1 Kim YS, "Vascular endothelial growth factor is a key mediator in the development of T cell priming and its polarization to type 1 and type 17 T helper cells in the airways" 183 : 5113-5120, 2009

      2 Ivanov II, "The orphan nuclear receptor RORgt directs the differentiation program of proinflammatory IL-17þ T helper cells" 126 : 1121-11233, 2006

      3 Yin M-J, "The anti-inflammatory agents aspirin and salicylate inhibit the activityof IkB kinase-b" 396 : 77-80, 1998

      4 Qian Y, "The adaptor Act1 is required for interleukin 17-dependent signaling associated with autoimmune and inflammatory disease" 8 : 247-256, 2007

      5 Soroosh P, "Th9 and allergic disease" 127 : 450-458, 2009

      6 Schwenger P, "Sodium salicylate induces apoptosis via p38 mitogen-activated protein kinase but inhibits tumor necrosis factor-induced c-Jun N-terminal kinase/stressactivated protein kinase activation" 94 : 2869-2873, 1997

      7 Chang SH, "Signaling of interleukin-17 family cytokines in immunity and inflammation" 23 : 1069-1075, 2011

      8 Cronstein BN, "Salicylates and sulfasalazine, but not glucocorticoids, inhibit leukocyte accumulation by an adenosine-dependent mechanism that is independent of inhibition of prostaglandin synthesis and p105 of NFkappaB" 96 : 6377-6381, 1999

      9 Scott MJ, "STATs, cytokines, and sepsis" 9 : 1153-1159, 2002

      10 Yuan ZL, "STAT3 dimerization regulated by reversible actylation of a single lysine residue" 307 : 269-273, 2005

      1 Kim YS, "Vascular endothelial growth factor is a key mediator in the development of T cell priming and its polarization to type 1 and type 17 T helper cells in the airways" 183 : 5113-5120, 2009

      2 Ivanov II, "The orphan nuclear receptor RORgt directs the differentiation program of proinflammatory IL-17þ T helper cells" 126 : 1121-11233, 2006

      3 Yin M-J, "The anti-inflammatory agents aspirin and salicylate inhibit the activityof IkB kinase-b" 396 : 77-80, 1998

      4 Qian Y, "The adaptor Act1 is required for interleukin 17-dependent signaling associated with autoimmune and inflammatory disease" 8 : 247-256, 2007

      5 Soroosh P, "Th9 and allergic disease" 127 : 450-458, 2009

      6 Schwenger P, "Sodium salicylate induces apoptosis via p38 mitogen-activated protein kinase but inhibits tumor necrosis factor-induced c-Jun N-terminal kinase/stressactivated protein kinase activation" 94 : 2869-2873, 1997

      7 Chang SH, "Signaling of interleukin-17 family cytokines in immunity and inflammation" 23 : 1069-1075, 2011

      8 Cronstein BN, "Salicylates and sulfasalazine, but not glucocorticoids, inhibit leukocyte accumulation by an adenosine-dependent mechanism that is independent of inhibition of prostaglandin synthesis and p105 of NFkappaB" 96 : 6377-6381, 1999

      9 Scott MJ, "STATs, cytokines, and sepsis" 9 : 1153-1159, 2002

      10 Yuan ZL, "STAT3 dimerization regulated by reversible actylation of a single lysine residue" 307 : 269-273, 2005

      11 Gao H, "STAT3 and suppressor of cytokine signaling 3: potential targets in lung inflammatory responses" 11 : 869-880, 2007

      12 Jetten AM, "Retinoid-related orphan receptors (RORs): critical roles in development, immunity, circadian rhythm, and cellular metabolism" 7 : 1-32, 2009

      13 Yang XP, "Opposing regulation of the locus encoding IL-17 through direct, reciprocal actions of STAT3 and STAT5" 12 : 247-254, 2011

      14 Ohbayashi N, "LIF- and IL-6-induced acetylation of STAT3 at Lys-685 through PI3K/Akt activation" 30 : 1860-, 2007

      15 Zhao L, "Interleukin-17 contributes to the pathogenesis of autoimmune hepatitis through inducing hepatic interleukin-6 expression" 19 : e18909-, 2011

      16 Sutton CE, "Interleukin-1 and IL-23 induce innate IL-17 production from gd T cells, amplifying Th17 responses and autoimmunity" 31 : 331-341, 2009

      17 Vane JR, "Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs" 231 : 232-235, 1971

      18 Zepp J, "IL-17 receptor signaling and T helper 17-mediated autoimmune demyelinating disease" 32 : 232-239, 2011

      19 Weaver CT, "IL-17 family cytokiens and the expanding diversity of effector T cell leneages" 25 : 821-852, 2007

      20 Korn T, "IL-17 and Th17 cells" 27 : 485-517, 2009

      21 Bateman ED, "Global strategy for asthma management and prevention: GINA executive summary" 31 : 143-178, 2008

      22 Francesco F, "Do studies in humans better depict Th17 cells?" 114 : 2213-2219, 2009

      23 Moon HG, "Conversion of Th17-type into Th2-type inflammation by acetyl salicylic acid via the adenosine and uric acid pathway in the lung" 65 : 1093-1103, 2010

      24 Busse WW, "Asthma" 344 : 350-362, 2001

      25 Cla`ria J, "Aspirin triggers previously undescribed bioactive eicosanoids by human endothelial cell-leukocyte interactions" 92 : 9475-9479, 1995

      26 Guermonprez P, "Antigen presentation and T cell stimulation by dendritic cells" 20 : 621-667, 2002

      27 Lutz MB, "An advanced culture method for generating large quantities of highly pure dendritic cells from mouse bone marrow" 223 : 77-92, 1999

      28 Kim YK, "Airway exposure levels of lipopolysaccharide determine type 1 versus type 2 experimental asthma" 178 : 5375-5382, 2007

      29 Park H, "A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17" 6 : 1133-1141, 2005

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      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2023 평가예정 해외DB학술지평가 신청대상 (해외등재 학술지 평가)
      2020-01-01 평가 등재학술지 유지 (해외등재 학술지 평가) KCI등재
      2009-09-21 학회명변경 한글명 : 대한생화학ㆍ분자생물학회 -> 생화학분자생물학회
      영문명 : Korean Society Of Medical Biochemistry And Molecular Biology -> Korean Society Of Biochemistry And Molecular Biology
      KCI등재
      2008-01-01 평가 SCI 등재 (등재유지) KCI등재
      2006-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2004-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2001-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      1998-07-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 3.74 0.23 2.56
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      1.82 1.45 0.555 0.01
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