Staphylococcus Enterotoxin a Induces Muc5B Expression Via Toll-Like Receptor 2, Extracellular Signal–Regulated Kinase 1/2, and P38 Mitogen-Activated Protein Kinase in Human Airway Epithelial Cells

2014 ◽  
Vol 28 (1) ◽  
pp. e25-e30 ◽  
Author(s):  
Si-Youn Song ◽  
Deok Hwan Chi ◽  
Chang Hoon Bae ◽  
Yong-Dae Kim
Keyword(s):  
Protein Kinase ◽  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Mitogen Activated Protein Kinase ◽  
Airway Epithelial ◽  
Toll Like Receptor ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Mitogen Activated Protein ◽  
Toll Like Receptor 2

scholarly journals Treponema denticola Activates Mitogen-Activated Protein Kinase Signal Pathways through Toll-Like Receptor 2

2007 ◽  
Vol 75 (12) ◽  
pp. 5763-5768 ◽  
Author(s):  
John Ruby ◽  
Kunal Rehani ◽  
Michael Martin
Keyword(s):  
Protein Kinase ◽  
Mapk Signaling ◽  
Innate Immune ◽  
Mitogen Activated Protein Kinase ◽  
Signal Pathways ◽  
Treponema Denticola ◽  
Toll Like Receptor ◽  
Extracellular Signal ◽  
Mitogen Activated Protein ◽  
Toll Like Receptor 2

ABSTRACT Treponema denticola, a spirochete indigenous to the oral cavity, is associated with host inflammatory responses to anaerobic polymicrobial infections of the root canal, periodontium, and alveolar bone. However, the cellular mechanisms responsible for the recognition of T. denticola by the innate immune system and the underlying cell signaling pathways that regulate the inflammatory response to T. denticola are currently unresolved. In this study, we demonstrate that T. denticola induces innate immune responses via the utilization of Toll-like receptor 2 (TLR2) but not TLR4. Assessment of TLR2/1 and TLR2/6 heterodimers revealed that T. denticola predominantly utilizes TLR2/6 for the induction of cellular responses. Analysis of the mitogen-activated protein kinase (MAPK) signaling pathway in T. denticola-stimulated monocytes identified a prolonged up-regulation of the MAPK extracellular signal-related kinase 1/2 (ERK1/2) and p38, while no discernible increase in phospho-c-Jun N-terminal kinase 1/2 (JNK1/2) levels was observed. With the aid of pharmacological inhibitors selectively targeting ERK1/2 via the mitogen-activated protein kinase/extracellular signal-related kinase 1/2 kinase and p38, we further demonstrate that ERK1/2 and p38 play a major role in T. denticola-mediated pro- and anti-inflammatory cytokine production.

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