Distinct Involvement Of P38 MAPK In Up-Regulation Of Interleukin-8 In Monocyte-Derived Macrophages And Airway Epithelial Cells Stimulated With Lipopolysaccharide Or Interleukin-1Beta

Author(s):  
Nurlan Dauletbaev ◽  
Kassey Herscovitch ◽  
Maria Cammisano ◽  
Larry C. Lands
2005 ◽  
Vol 175 (8) ◽  
pp. 5333-5340 ◽  
Author(s):  
Paul T. G. Elkington ◽  
Jenny E. Emerson ◽  
Laura D. C. Lopez-Pascua ◽  
Cecilia M. O’Kane ◽  
Donna E. Horncastle ◽  
...  

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Catherine M. Greene ◽  
Hugh Ramsay ◽  
Robert J. Wells ◽  
Shane J. O'Neill ◽  
Noel G. McElvaney

Cystic Fibrosis (CF) is an inherited disorder characterised by chronic inflammation of the airways. The lung manifestations of CF include colonization withPseudomonas aeruginosaandStaphylococcus aureusleading to neutrophil-dominated airway inflammation and tissue damage. Inflammation in the CF lung is initiated by microbial components which activate the innate immune response via Toll-like receptors (TLRs), increasing airway epithelial cell production of proinflammatory mediators such as the neutrophil chemokine interleukin-8 (IL-8). Thus modulation of TLR function represents a therapeutic approach for CF. Nicotine is a naturally occurring plant alkaloid. Although it is negatively associated with cigarette smoking and cardiovascular damage, nicotine also has anti-inflammatory properties. Here we investigate the inhibitory capacity of nicotine against TLR2- and TLR4-induced IL-8 production by CFTE29o- airway epithelial cells, determine the role ofα7-nAChR (nicotinic acetylcholine receptor) in these events, and provide data to support the potential use of safe nicotine analogues as anti-inflammatories for CF.


1994 ◽  
Vol 93 (1) ◽  
pp. 26-32 ◽  
Author(s):  
P P Massion ◽  
H Inoue ◽  
J Richman-Eisenstat ◽  
D Grunberger ◽  
P G Jorens ◽  
...  

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