The IL-8 production by streptococcal pyrogenic exotoxin B

Chia Wen Chang, Siang Yu Wu, Woei-Jer Chuang, Yee-Shin Lin, S. Y. Wu, Ching-Chuan Liu, Pei-Jane Tsai, Ming T. Lin

研究成果: Article

4 引文 (Scopus)

摘要

We have previously identified αvβ3 and Fas as receptors for the streptococcal pyrogenic exotoxin B (SPE B), and G308S, a mutant of SPE B with RSD motif, which interacts with Fas only. This study aims to evaluate how SPE B interacts with cells to induce the production of IL-8. Our results showed that following exposure to SPE B or G308S, the levels of IL-8 protein and mRNA were increased and the increase was inhibited by the addition of anti-Fas antibody, suggesting that the increased production of IL-8 by SPE B is mediated through Fas receptor. In the presence of G308S, the association of FADD and procaspase 8, and activation of NF-κB were also detected. The application of siRNA of FADD and of procaspase 8 could inhibit the NF-κB activity. The proteolytic activity of caspase 8 was required for the NF-κB activity. Further studies showed that G308S could increase the phosphorylation of ERK and the translocation of NF-κB into the nucleus, and the inhibition of ERK phosphorylation decreased the IL-8 production, mRNA expression and activation of NF-κB. In addition, siRNA of procaspase 8 could inhibit the G308S-induced cleavage of MEKK1, binding of MEKK1 to caspase 8, activation of ERK and the NF-κB activity. Taken together, the production of IL-8 by SPE B in A549 cells is mediated by Fas, and followed by the activation of FADD, caspase 8, MEKK1, ERK and NF-κB.

原文English
頁(從 - 到)1316-1326
頁數11
期刊Experimental Biology and Medicine
234
發行號11
DOIs
出版狀態Published - 2009 十一月 1

指紋

Caspase 8
Interleukin-8
Chemical activation
CD95 Antigens
Phosphorylation
Small Interfering RNA
Messenger RNA
erythrogenic toxin
Anti-Idiotypic Antibodies
Association reactions
Antibodies
Proteins

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)

引用此文

Chang, Chia Wen ; Wu, Siang Yu ; Chuang, Woei-Jer ; Lin, Yee-Shin ; Wu, S. Y. ; Liu, Ching-Chuan ; Tsai, Pei-Jane ; Lin, Ming T. / The IL-8 production by streptococcal pyrogenic exotoxin B. 於: Experimental Biology and Medicine. 2009 ; 卷 234, 編號 11. 頁 1316-1326.
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The IL-8 production by streptococcal pyrogenic exotoxin B. / Chang, Chia Wen; Wu, Siang Yu; Chuang, Woei-Jer; Lin, Yee-Shin; Wu, S. Y.; Liu, Ching-Chuan; Tsai, Pei-Jane; Lin, Ming T.

於: Experimental Biology and Medicine, 卷 234, 編號 11, 01.11.2009, p. 1316-1326.

研究成果: Article

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T1 - The IL-8 production by streptococcal pyrogenic exotoxin B

AU - Chang, Chia Wen

AU - Wu, Siang Yu

AU - Chuang, Woei-Jer

AU - Lin, Yee-Shin

AU - Wu, S. Y.

AU - Liu, Ching-Chuan

AU - Tsai, Pei-Jane

AU - Lin, Ming T.

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AB - We have previously identified αvβ3 and Fas as receptors for the streptococcal pyrogenic exotoxin B (SPE B), and G308S, a mutant of SPE B with RSD motif, which interacts with Fas only. This study aims to evaluate how SPE B interacts with cells to induce the production of IL-8. Our results showed that following exposure to SPE B or G308S, the levels of IL-8 protein and mRNA were increased and the increase was inhibited by the addition of anti-Fas antibody, suggesting that the increased production of IL-8 by SPE B is mediated through Fas receptor. In the presence of G308S, the association of FADD and procaspase 8, and activation of NF-κB were also detected. The application of siRNA of FADD and of procaspase 8 could inhibit the NF-κB activity. The proteolytic activity of caspase 8 was required for the NF-κB activity. Further studies showed that G308S could increase the phosphorylation of ERK and the translocation of NF-κB into the nucleus, and the inhibition of ERK phosphorylation decreased the IL-8 production, mRNA expression and activation of NF-κB. In addition, siRNA of procaspase 8 could inhibit the G308S-induced cleavage of MEKK1, binding of MEKK1 to caspase 8, activation of ERK and the NF-κB activity. Taken together, the production of IL-8 by SPE B in A549 cells is mediated by Fas, and followed by the activation of FADD, caspase 8, MEKK1, ERK and NF-κB.

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