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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

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.

Authors:
 [1];  [1];  [1];  [1];  [1];  [1];  [2]
  1. Inserm, U719, Paris, F-75012 (France)
  2. Inserm, U719, Paris, F-75012 (France) and Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 (France)
Publication Date:
OSTI Identifier:
20991366
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 357; Journal Issue: 2; Other Information: DOI: 10.1016/j.bbrc.2007.03.141; PII: S0006-291X(07)00633-X; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; FIBROSIS; INFLAMMATION; LUNGS; PATIENTS; PHOSPHOTRANSFERASES; STIMULATION; TRANSCRIPTION

Citation Formats

Muselet-Charlier, Celine, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012, Roque, Telma, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012, Boncoeur, Emilie, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012, Chadelat, Katarina, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012, AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012, Clement, Annick, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012, AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012, Jacquot, Jacky, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012, 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, Roque, Telma, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012, Boncoeur, Emilie, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012, Chadelat, Katarina, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012, AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012, Clement, Annick, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012, AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012, Jacquot, Jacky, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012, & 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, Roque, Telma, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012, Boncoeur, Emilie, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012, Chadelat, Katarina, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012, AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012, Clement, Annick, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012, AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012, Jacquot, Jacky, Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012, 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.
@article{osti_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 and Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 and Roque, Telma and Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 and Boncoeur, Emilie and Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 and Chadelat, Katarina and Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 and AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012 and Clement, Annick and Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 and AP-HP, Hopital Trousseau, Pediatric Pulmonary Department, Paris, F-75012 and Jacquot, Jacky and Universite Pierre et Marie Curie-Paris 6, Paris, UMR-S719, F-75012 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},
url = {https://www.osti.gov/biblio/20991366}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 2,
volume = 357,
place = {United States},
year = {Fri Jun 01 00:00:00 EDT 2007},
month = {Fri Jun 01 00:00:00 EDT 2007}
}