scholarly journals Social Stress Enhances Allergen-Induced Airway Inflammation in Mice and Inhibits Corticosteroid Responsiveness of Cytokine Production

2009 ◽  
Vol 182 (12) ◽  
pp. 7888-7896 ◽  
Author(s):  
Michael T. Bailey ◽  
Sonja Kierstein ◽  
Satish Sharma ◽  
Matthew Spaits ◽  
Steven G. Kinsey ◽  
...  
2009 ◽  
Vol 183 (5) ◽  
pp. 3551.2-3551
Author(s):  
M. T. Bailey ◽  
S. Kierstein ◽  
S. Sharma ◽  
M. Spaits ◽  
S. G. Kinsey ◽  
...  

2017 ◽  
Vol 214 (10) ◽  
pp. 3037-3050 ◽  
Author(s):  
Takashi Ito ◽  
Koichi Hirose ◽  
Aiko Saku ◽  
Kenta Kono ◽  
Hiroaki Takatori ◽  
...  

Previous studies have shown that IL-22, one of the Th17 cell–related cytokines, plays multiple roles in regulating allergic airway inflammation caused by antigen-specific Th2 cells; however, the underlying mechanism remains unclear. Here, we show that allergic airway inflammation and Th2 and Th17 cytokine production upon intratracheal administration of house dust mite (HDM) extract, a representative allergen, were exacerbated in IL-22-deficient mice. We also found that IL-22 induces Reg3γ production from lung epithelial cells through STAT3 activation and that neutralization of Reg3γ significantly exacerbates HDM-induced eosinophilic airway inflammation and Th2 cytokine induction. Moreover, exostatin-like 3 (EXTL3), a functional Reg3γ binding protein, is expressed in lung epithelial cells, and intratracheal administration of recombinant Reg3γ suppresses HDM-induced thymic stromal lymphopoietin and IL-33 expression and accumulation of type 2 innate lymphoid cells in the lung. Collectively, these results suggest that IL-22 induces Reg3γ production from lung epithelial cells and inhibits the development of HDM-induced allergic airway inflammation, possibly by inhibiting cytokine production from lung epithelial cells.


2002 ◽  
Vol 109 (1) ◽  
pp. S294-S295
Author(s):  
David Quarcoo ◽  
Silke Weixler ◽  
Philippe Stock ◽  
Kerstin Gerhold ◽  
S Hader ◽  
...  

Cytokine ◽  
2013 ◽  
Vol 61 (1) ◽  
pp. 237-244 ◽  
Author(s):  
Yu-Tzu Lee ◽  
Shiuan-Shinn Lee ◽  
Hai-Lun Sun ◽  
Ko-Hsiu Lu ◽  
Min-Sho Ku ◽  
...  

2010 ◽  
Vol 33 (5) ◽  
pp. 780-783 ◽  
Author(s):  
Tokuyuki Yoshida ◽  
Yasuo Yoshioka ◽  
Maho Fujimura ◽  
Hiroyuki Kayamuro ◽  
Kohei Yamashita ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Ju Hee Lee ◽  
Hun Jai Lim ◽  
Chan Woo Lee ◽  
Kun-Ho Son ◽  
Jong-Keun Son ◽  
...  

The present study was designed to find pharmacologically active compound against airway inflammation from the roots ofAsparagus cochinchinensis. The 70% ethanol extract of the roots ofA. cochinchinensis(ACE) was found to inhibit IL-6 production from IL-1β-treated lung epithelial cells (A549) and the major constituent, methyl protodioscin (MP), also strongly inhibited the production of IL-6, IL-8, and tumor necrosis factor- (TNF-)αfrom A549 cells at 10–100 μM. This downregulating effect of proinflammatory cytokine production was found to be mediated, at least in part, via inhibition of c-Jun N-terminal kinase (JNK) and c-Jun activation pathway. When examined on anin vivomodel of airway inflammation in mice, lipopolysaccharide- (LPS-) induced acute lung injury, ACE, and MP significantly inhibited cell infiltration in the bronchoalveolar lavage fluid by the oral treatment at doses of 100–400 mg/kg and 30–60 mg/kg, respectively. MP also inhibited the production of proinflammatory cytokines such as IL-6, TNF-α, and IL-1βin lung tissue. All of these findings provide scientific evidence supporting the role ofA. cochinchinensisas a herbal remedy in treating airway inflammation and also suggest a therapeutic value of MP on airway inflammatory disorders.


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