scholarly journals The Level of p38α Mitogen-Activated Protein Kinase Activation in Airway Epithelial Cells Determines the Onset of Innate Immune Responses to Planktonic and Biofilm Pseudomonas aeruginosa

2013 ◽  
Vol 207 (10) ◽  
pp. 1544-1555 ◽  
Author(s):  
Trevor Beaudoin ◽  
Shantelle LaFayette ◽  
Lucie Roussel ◽  
Julie Bérubé ◽  
Martin Desrosiers ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Immune Responses ◽  
Airway Epithelial Cells ◽  
Innate Immune ◽  
Mitogen Activated Protein Kinase ◽  
Airway Epithelial ◽  
Innate Immune Responses ◽  
Kinase Activation ◽  
Protein Kinase Activation ◽  
Mitogen Activated Protein

scholarly journals The p38 Mitogen-Activated Protein Kinase Signaling Pathway Is Coupled to Toll-Like Receptor 5 To Mediate Gene Regulation in Response to Pseudomonas aeruginosa Infection in Human Airway Epithelial Cells

2007 ◽  
Vol 75 (12) ◽  
pp. 5985-5992 ◽  
Author(s):  
Zhe Zhang ◽  
William Reenstra ◽  
Daniel J. Weiner ◽  
Jean-Pierre Louboutin ◽  
James M. Wilson
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Gene Regulation ◽  
P38 Mapk ◽  
Airway Epithelial Cells ◽  
Mitogen Activated Protein Kinase ◽  
Airway Epithelial ◽  
Toll Like Receptor ◽  
Mapk Activation ◽  
Mitogen Activated Protein ◽  
Toll Like Receptor 5

ABSTRACT In this study, we show that stimulation of human airway epithelial cells (HAECs) by Pseudomonas aeruginosa strain PAO1 induces time- and dose-dependent activation of p38 mitogen-activated protein kinase (MAPK). Activated p38 MAPK stayed in the cytoplasm instead of translocating to the nucleus, as shown by cellular fractionation. p38 MAPK was activated when HAECs were incubated with P. aeruginosa strain PAK and Burkholderia cepacia, while little activation was observed with the isogenic flagellin-free strains PAK/fliC and B. cepacia BC/fliC. The presence of Toll-like receptor 5 (TLR5) in 293 cells mediated PAO1-dependent activation of p38 MAPK, and in HAECs p38 MAPK activation was blocked by the overexpression of a dominant negative TLR5. Two inhibitors of p38 MAPK, SB202190 and SB203580, significantly attenuated PAO1-dependent expression of an NF-κB-dependent luciferase reporter gene, suggesting that p38 MAPK activation is required for full activation of NF-κB-dependent signaling. Microarray analysis of NF-κB target genes revealed up-regulation of multiple genes by PAO1 in HAECs. Reverse transcription-PCR and protein expression analysis were used to show that up-regulation of NF-κB-dependent genes induced by PAO1, such as the genes encoding Cox-2 and interleukin-8, was attenuated by SB203580. These results demonstrate a role for p38 MAPK signaling in gene regulation in response to P. aeruginosa via TLR5.

Dual-specificity phosphatase 1: a critical regulator of innate immune responses

2006 ◽  
Vol 34 (6) ◽  
pp. 1018-1023 ◽  
Author(s):  
S.M. Abraham ◽  
A.R. Clark
Keyword(s):  
Innate Immunity ◽  
Immune Responses ◽  
P38 Mapk ◽  
Time Course ◽  
Inflammatory Diseases ◽  
Innate Immune ◽  
Mitogen Activated Protein Kinase ◽  
Innate Immune Responses ◽  
Inflammatory Stimuli ◽  
Mitogen Activated Protein

Innate immune responses are critically dependent on MAPK (mitogen-activated protein kinase) signalling pathways, in particular JNK (c-Jun N-terminal kinase) and p38 MAPK. Both of these kinases are negatively regulated via their dephosphorylation by DUSP1 (dual­-specificity phosphatase 1). Several pro- and anti-inflammatory stimuli converge to regulate the DUSP1 gene and to modulate the time course of its expression. In turn, the pattern of expression of DUSP1 dictates the kinetics of activation of JNK and p38 MAPK, and this influences the expression of several mediators of innate immunity. DUSP1 is therefore a central regulator of innate immunity, and its expression can profoundly affect the outcome of inflammatory challenges. We discuss possible implications for immune-mediated inflammatory diseases and their treatment.

scholarly journals Enhanced Toll-Like Receptor Responsiveness Associated with Mitogen-Activated Protein Kinase Activation in Plasmodium falciparum-Infected Children

2008 ◽  
Vol 76 (11) ◽  
pp. 5149-5157 ◽  
Author(s):  
Franca C. Hartgers ◽  
Benedicta B. Obeng ◽  
Astrid Voskamp ◽  
Irene A. Larbi ◽  
Abena S. Amoah ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Protein Kinase ◽  
Mononuclear Cells ◽  
Innate Immune ◽  
Mitogen Activated Protein Kinase ◽  
Peripheral Blood Mononuclear ◽  
Kinase Activation ◽  
Protein Kinase Activation ◽  
Mitogen Activated Protein

ABSTRACT Acute Plasmodium falciparum infection is associated with strongly upregulated cytokine responses that are at least partly the result of activation of Toll-like receptors (TLRs). Whether and how TLR expression/responsiveness changes upon malarial infection is, however, currently not well understood. To assess this, we examined expression of TLRs and used the TLR ligand lipopolysaccharide (LPS) and Pam3Cys to stimulate peripheral blood mononuclear cells (PBMCs) from Ghanaian schoolchildren who live in a rural area where P. falciparum is endemic. Expression of TLR2 was higher, and responses to its ligand, Pam3Cys, were enhanced in P. falciparum-infected children compared to their uninfected counterparts. In cells from the same children, stimulation by Pam3Cys resulted in higher p38 mitogen-activated protein kinase activation and higher cytokine production. In vitro experiments confirmed that preincubation of PBMCs with P. falciparum-infected red blood cells enhanced responsiveness to TLR ligands. Taken together, the data indicate that P. falciparum-infected children in areas where malaria is endemic have an altered innate immune system, which might be important for the balance between immunity and pathology when new infections are encountered or when novel vaccines are introduced.

scholarly journals Viral and host factors determine innate immune responses in airway epithelial cells from children with wheeze and atopy

Thorax ◽  
2014 ◽  
Vol 69 (10) ◽  
pp. 918-925 ◽  
Author(s):  
Kirsten M Spann ◽  
Engin Baturcam ◽  
Johanna Schagen ◽  
Carmen Jones ◽  
Claire P Straub ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Immune Responses ◽  
Airway Epithelial Cells ◽  
Innate Immune ◽  
Host Factors ◽  
Airway Epithelial ◽  
Innate Immune Responses
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