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20231223072008.0 |
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231223s2005 xx ||||| 00| ||eng c |
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|a pubmed24n0518.xml
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|a (DE-627)NLM155374907
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|a (NLM)15893694
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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100 |
1 |
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|a Rahman, M S
|e verfasserin
|4 aut
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245 |
1 |
0 |
|a IL-17R activation of human airway smooth muscle cells induces CXCL-8 production via a transcriptional-dependent mechanism
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264 |
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1 |
|c 2005
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336 |
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|a Text
|b txt
|2 rdacontent
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337 |
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|a ohne Hilfsmittel zu benutzen
|b n
|2 rdamedia
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338 |
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|a Band
|b nc
|2 rdacarrier
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500 |
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|a Date Completed 14.07.2005
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|a Date Revised 21.11.2008
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|a published: Print
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|a Citation Status MEDLINE
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520 |
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|a Airway neutrophilia has been recognized as a predominant feature of acute lung disorders. While it has been shown that IL-17 induces expression of the CXC chemokines in the airways leading to neutrophil recruitment, the IL-17R expression in human ASM cells and the molecular mechanism by which IL-17 mediates neutrophilic chemo-attractant CXCL-8 (IL-8) production have not been determined. Our study showed that ASM cells express steady state IL-17R protein, mRNA and surface-bound receptor. Interestingly, airway sections from COPD patients revealed IL-17R-positive immunostaining within ASM bundles. IL-17 was capable of stimulating CXCL-8 protein release from ASM cells which was significantly decreased by neutralizing anti-IL-17 mAb. Furthermore, IL-17 induction of CXCL-8 mRNA and protein release from ASM cells was abrogated by transcriptional inhibitor actinomycin D. CXCL-8 promoter reporter analysis using wild type and site specific mutant constructs demonstrated a key role for AP1 and NF-kappaB binding sites in IL-17-induced CXCL-8 expression. These data demonstrate that IL-17 mediates CXCL-8 expression in ASM cells via a transcriptional mechanism depending on NF-kappaB and AP-1 pathways. Together, our findings suggest that ASM cells play an important role in airway neutrophilia
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4 |
|a Journal Article
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650 |
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4 |
|a Research Support, Non-U.S. Gov't
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650 |
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7 |
|a IL17RA protein, human
|2 NLM
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650 |
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7 |
|a Interleukin-17
|2 NLM
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650 |
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7 |
|a Interleukin-8
|2 NLM
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650 |
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7 |
|a RNA, Messenger
|2 NLM
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650 |
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7 |
|a Receptors, Interleukin
|2 NLM
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650 |
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7 |
|a Receptors, Interleukin-17
|2 NLM
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700 |
1 |
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|a Yang, Jie
|e verfasserin
|4 aut
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700 |
1 |
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|a Shan, Lian Yu
|e verfasserin
|4 aut
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700 |
1 |
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|a Unruh, Helmut
|e verfasserin
|4 aut
|
700 |
1 |
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|a Yang, Xi
|e verfasserin
|4 aut
|
700 |
1 |
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|a Halayko, Andrew J
|e verfasserin
|4 aut
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700 |
1 |
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|a Gounni, Abdelilah Soussi
|e verfasserin
|4 aut
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773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 115(2005), 3 vom: 31. Juni, Seite 268-76
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
|
773 |
1 |
8 |
|g volume:115
|g year:2005
|g number:3
|g day:31
|g month:06
|g pages:268-76
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912 |
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|a GBV_USEFLAG_A
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912 |
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|a SYSFLAG_A
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|a GBV_NLM
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912 |
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|a GBV_ILN_11
|
912 |
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|a GBV_ILN_24
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912 |
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|a GBV_ILN_350
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951 |
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|a AR
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952 |
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|d 115
|j 2005
|e 3
|b 31
|c 06
|h 268-76
|