Oxidative stress induces extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase in cystic fibrosis lung epithelial cells: Potential mechanism for excessive IL-8 expression

Boncoeur, Émilie; Saint‐Criq, Vinciane; Bonvin, Elise; Roque, Telma; Henrion‐Caude, Alexandra; Gruenert, Dieter C.; Clément, Annick; Jacquot, Jacky; Tabary, Olivier

doi:10.1016/j.biocel.2007.08.013

Cited by 41 publications

(24 citation statements)

References 63 publications

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“…The major phosphoproteins and nuclear transcription factors evidenced in this investigation are reported. Arrows with dashed lines indicate the putative interactions between the different phosphoproteins and transcription factors as obtained from the literature and described in the text (18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(37)(38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50)(51). Dashed arrows are related to the putative transmembrane signaling of P. aeruginosa (black lines), IL-1b (red lines), or TNF-a (blue lines).…”

Section: Discussionmentioning

confidence: 99%

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Mapping the Transcriptional Machinery of the IL-8 Gene in Human Bronchial Epithelial Cells

Bezzerri

Borgatti

Finotti

et al. 2011

The Journal of Immunology

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IL-8 released from bronchial epithelial cells infected with Pseudomonas aeruginosa plays a crucial role in the chronic lung pathology of patients affected by cystic fibrosis. Novel anti-inflammatory approaches will benefit from a thorough understanding of the regulatory mechanisms involved in the transcription of this chemokine to identify potential pharmacological targets. We addressed this issue by investigating the role of phosphoproteins and transcription factors (TFs) on transcription of IL-8 gene in the human bronchial epithelial IB3-1, CuFi-1, and Calu-3 cells. P. aeruginosa increased the basal phosphorylation of the ERK1/2 pathway components 90-kDa ribosomal S6 kinase (RSK)1/2 and mitogen- and stress-activated kinase-2 and of the p38 MAPK pathway components p38α/δ/γ and heat shock protein 27 (HSP27). The involvement of these kinases in the expression of IL-8 gene was confirmed with pharmacological inhibitors of ERK1/2, RSK, p38, and HSP27 both at transcription and secretion levels. Transfection of TF decoy oligodeoxynucleotides, designed to interfere with the interaction of the TFs NF-κB, NF-IL6, AP-1, CREB, and CHOP with the corresponding consensus sequences identified in the IL-8 promoter, reduced the P. aeruginosa-dependent transcription of IL-8, suggesting their participation in the transcriptional machinery. Stimulation of IB3-1 cells with IL-1β led to a similar pattern of activation, whereas the pattern of phosphoproteins and of TFs modulated by TNF-α differentiated sharply. In conclusion, the results highlight a novel role for RSK1/2 and HSP27 phosphoproteins and of the cooperative role of the TFs NF-κB, NF-IL6, AP-1, CHOP, and CREB in P. aeruginosa-dependent induction of transcription of the IL-8 gene in human bronchial epithelial cells.

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Section: Discussionmentioning

confidence: 99%

“…These phosphorylations eventually activate transcription factors (TFs), first of all NF-kB (22)(23)(24)(25)(26)(27)(28). Lung inflammation in CF has been related to an increased NF-kB signaling causing the induction of IL-8 gene expression (22,23,29).…”

mentioning

confidence: 99%

Mapping the Transcriptional Machinery of the IL-8 Gene in Human Bronchial Epithelial Cells

Bezzerri

Borgatti

Finotti

et al. 2011

The Journal of Immunology

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“…Activated neutrophils migrate to the airways and release large amounts of ROS. On the other hand in CF epithelial cells, antioxidant defense systems appear to be defective in their ability to control the amount of ROS produced [15]. Therefore over-abundance of ROS and their products may cause tissue injury-events and modify intracellular signalling pathways leading to cell apoptosis and enhanced inflammatory processes.…”

Section: Aerosolized Antioxidant and Anti-inflammatory Agents In Cystmentioning

confidence: 99%

Development and Investigation of Dry Powder Inhalers for Cystic Fibrosis

Russo¹,

Prota²,

Stigliani³

et al. 2012

Recent Advances in Novel Drug Carrier Systems

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“…The MAPK family of serine-threonine protein kinases is a highly conserved family consisting of three primary members; extracellular signal-related kinases (ERK), c-Jun amino-terminal kinases (JNK), and p38. MAPKs play an active signaling role following multiple stimuli, some of which include irradiation, osmotic stress, inflammation, growth factors, and mechanical loading (8)(9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

VSL#3 probiotics regulate the intestinal epithelial barrier inï¿½vivo and in vitro via the p38 and ERK signaling pathways

Jiang

2011

Int J Mol Med

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Abstract. Probiotics can play a role in enhancing intestinal barrier function. However, the underlying mechanisms are not fully understood. The aim of this study was to examine the effects of VSL#3 probiotics on colonic epithelium permeability, tight junction protein expression and MAPKs signaling pathways in vivo and in vitro. In vivo, acute colitis was induced by administration of 3.5% dextran sodium sulfate for 7 days. Rats in two groups were treated with either 15 mg VSL#3 or placebo via a gastric tube once daily after induction of colitis. Tight junction protein expression and the MAPKs signaling pathways were studied by immunohistochemistry and immunoblotting. In vitro, HT-29 cells were exposed to TNF-α for up to 48 h with or without pre-treatment with a p38 MAPK inhibitor, an ERK inhibitor or a JNK inhibitor. Then tight junction proteins and the phosphorylation of MAPKs were examined in the presence or absence of VSL#3. In vivo, VSL#3 probiotics significantly ameliorated the disease activity index from Day 4 onward. In acute colitis rats, decreased expression of the tight junction proteins were observed, whereas VSL#3 therapy prevented these changes and increased the expression of phosphorylated p38 (P-p38), and of phosphorylated ERK (P-ERK). In vitro, tight junction proteins, P-p38 and P-ERK in the VSL#3 group were significantly higher than in the control and TNF-α groups. The p38 MAPK inhibitor and the ERK inhibitor could effectively prevent this effect. VSL#3 probiotics protected the epithelial barrier and increased the tight junction protein expression in vivo and in vitro by activating the p38 and ERK signaling pathways.

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Oxidative stress induces extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase in cystic fibrosis lung epithelial cells: Potential mechanism for excessive IL-8 expression

Cited by 41 publications

References 63 publications

Mapping the Transcriptional Machinery of the IL-8 Gene in Human Bronchial Epithelial Cells

Mapping the Transcriptional Machinery of the IL-8 Gene in Human Bronchial Epithelial Cells

Development and Investigation of Dry Powder Inhalers for Cystic Fibrosis

VSL#3 probiotics regulate the intestinal epithelial barrier inï¿½vivo and in vitro via the p38 and ERK signaling pathways

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