Abstract
Transcription nuclear factor-{kappa}B (NF-{kappa}B) is hyperactivated in cystic fibrosis (CF) lung epithelial cells, and participates in exaggerated IL-8 production in the CF lung. We recently found that rapid activation of NF-{kappa}B occurred in a CF lung epithelial IB3-1 cell line (CF cells) upon IL-1{beta} stimulation, which was not observed in its CFTR-corrected lung epithelial S9 cell line (corrected cells). To test whether other signaling pathways such as that of mitogen-activated protein kinases (MAPKs) could be involved in IL-1{beta}-induced IL-8 production of CF cells, we investigated ERK1/2, JNK, and p38MAP signaling compared to NF-{kappa}B. Within 30 min, exposure to IL-1{beta} caused high activation of NF-{kappa}B, ERK1/2, p38MAP but not JNK in CF cells compared to corrected cells. Treatment of IL-1{beta}-stimulated CF cells with a series of chemical inhibitors of NF-{kappa}B, ERK1/2, and p38MAP, when used separately, reduced slightly IL-8 production. However, when used together, these inhibitors caused a blockade in IL-1{beta}-induced IL-8 production in CF cells. Understanding of the cross-talk between NF-{kappa}B and MAPKs signaling in CF lung epithelial cells may help in developing new therapeutics to reduce lung inflammation in patients with CF.
Muselet-Charlier, Celine;
[1]
Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)];
Roque, Telma;
[1]
Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)];
Boncoeur, Emilie;
[1]
Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)];
Chadelat, Katarina;
[1]
Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France);
AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012 (France)];
Clement, Annick;
[1]
Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France);
AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012 (France)];
Jacquot, Jacky;
[1]
Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)];
Tabary, Olivier
[2]
- Inserm, U719, Paris, F-75012 (France)
- Inserm, U719, Paris, F-75012 (France) and Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)
Citation Formats
Muselet-Charlier, Celine, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], Roque, Telma, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], Boncoeur, Emilie, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], Chadelat, Katarina, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France), AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012 (France)], Clement, Annick, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France), AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012 (France)], Jacquot, Jacky, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], and Tabary, Olivier.
Enhanced IL-1{beta}-induced IL-8 production in cystic fibrosis lung epithelial cells is dependent of both mitogen-activated protein kinases and NF-{kappa}B signaling.
United States: N. p.,
2007.
Web.
doi:10.1016/j.bbrc.2007.03.141.
Muselet-Charlier, Celine, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], Roque, Telma, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], Boncoeur, Emilie, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], Chadelat, Katarina, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France), AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012 (France)], Clement, Annick, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France), AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012 (France)], Jacquot, Jacky, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], & Tabary, Olivier.
Enhanced IL-1{beta}-induced IL-8 production in cystic fibrosis lung epithelial cells is dependent of both mitogen-activated protein kinases and NF-{kappa}B signaling.
United States.
https://doi.org/10.1016/j.bbrc.2007.03.141
Muselet-Charlier, Celine, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], Roque, Telma, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], Boncoeur, Emilie, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], Chadelat, Katarina, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France), AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012 (France)], Clement, Annick, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France), AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012 (France)], Jacquot, Jacky, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], and Tabary, Olivier.
2007.
"Enhanced IL-1{beta}-induced IL-8 production in cystic fibrosis lung epithelial cells is dependent of both mitogen-activated protein kinases and NF-{kappa}B signaling."
United States.
https://doi.org/10.1016/j.bbrc.2007.03.141.
@misc{etde_20991366,
title = {Enhanced IL-1{beta}-induced IL-8 production in cystic fibrosis lung epithelial cells is dependent of both mitogen-activated protein kinases and NF-{kappa}B signaling}
author = {Muselet-Charlier, Celine, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], Roque, Telma, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], Boncoeur, Emilie, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], Chadelat, Katarina, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France), AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012 (France)], Clement, Annick, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France), AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012 (France)], Jacquot, Jacky, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], and Tabary, Olivier}
abstractNote = {Transcription nuclear factor-{kappa}B (NF-{kappa}B) is hyperactivated in cystic fibrosis (CF) lung epithelial cells, and participates in exaggerated IL-8 production in the CF lung. We recently found that rapid activation of NF-{kappa}B occurred in a CF lung epithelial IB3-1 cell line (CF cells) upon IL-1{beta} stimulation, which was not observed in its CFTR-corrected lung epithelial S9 cell line (corrected cells). To test whether other signaling pathways such as that of mitogen-activated protein kinases (MAPKs) could be involved in IL-1{beta}-induced IL-8 production of CF cells, we investigated ERK1/2, JNK, and p38MAP signaling compared to NF-{kappa}B. Within 30 min, exposure to IL-1{beta} caused high activation of NF-{kappa}B, ERK1/2, p38MAP but not JNK in CF cells compared to corrected cells. Treatment of IL-1{beta}-stimulated CF cells with a series of chemical inhibitors of NF-{kappa}B, ERK1/2, and p38MAP, when used separately, reduced slightly IL-8 production. However, when used together, these inhibitors caused a blockade in IL-1{beta}-induced IL-8 production in CF cells. Understanding of the cross-talk between NF-{kappa}B and MAPKs signaling in CF lung epithelial cells may help in developing new therapeutics to reduce lung inflammation in patients with CF.}
doi = {10.1016/j.bbrc.2007.03.141}
journal = []
issue = {2}
volume = {357}
place = {United States}
year = {2007}
month = {Jun}
}
title = {Enhanced IL-1{beta}-induced IL-8 production in cystic fibrosis lung epithelial cells is dependent of both mitogen-activated protein kinases and NF-{kappa}B signaling}
author = {Muselet-Charlier, Celine, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], Roque, Telma, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], Boncoeur, Emilie, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], Chadelat, Katarina, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France), AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012 (France)], Clement, Annick, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France), AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012 (France)], Jacquot, Jacky, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)], and Tabary, Olivier}
abstractNote = {Transcription nuclear factor-{kappa}B (NF-{kappa}B) is hyperactivated in cystic fibrosis (CF) lung epithelial cells, and participates in exaggerated IL-8 production in the CF lung. We recently found that rapid activation of NF-{kappa}B occurred in a CF lung epithelial IB3-1 cell line (CF cells) upon IL-1{beta} stimulation, which was not observed in its CFTR-corrected lung epithelial S9 cell line (corrected cells). To test whether other signaling pathways such as that of mitogen-activated protein kinases (MAPKs) could be involved in IL-1{beta}-induced IL-8 production of CF cells, we investigated ERK1/2, JNK, and p38MAP signaling compared to NF-{kappa}B. Within 30 min, exposure to IL-1{beta} caused high activation of NF-{kappa}B, ERK1/2, p38MAP but not JNK in CF cells compared to corrected cells. Treatment of IL-1{beta}-stimulated CF cells with a series of chemical inhibitors of NF-{kappa}B, ERK1/2, and p38MAP, when used separately, reduced slightly IL-8 production. However, when used together, these inhibitors caused a blockade in IL-1{beta}-induced IL-8 production in CF cells. Understanding of the cross-talk between NF-{kappa}B and MAPKs signaling in CF lung epithelial cells may help in developing new therapeutics to reduce lung inflammation in patients with CF.}
doi = {10.1016/j.bbrc.2007.03.141}
journal = []
issue = {2}
volume = {357}
place = {United States}
year = {2007}
month = {Jun}
}