scholarly journals Serum amyloid A opposes lipoxin A4 to mediate glucocorticoid refractory lung inflammation in chronic obstructive pulmonary disease

2012 ◽  
Vol 109 (3) ◽  
pp. 935-940 ◽  
Author(s):  
S. Bozinovski ◽  
M. Uddin ◽  
R. Vlahos ◽  
M. Thompson ◽  
J. L. McQualter ◽  
...  
Author(s):  
Marta Maskey-Warzęchowska ◽  
Renata Rubinsztajn ◽  
Tadeusz Przybyłowski ◽  
Krzysztof Karwat ◽  
Patrycja Nejman-Gryz ◽  
...  

2008 ◽  
Vol 177 (3) ◽  
pp. 269-278 ◽  
Author(s):  
Steven Bozinovski ◽  
Anastasia Hutchinson ◽  
Michelle Thompson ◽  
Lochlan MacGregor ◽  
James Black ◽  
...  

Molecules ◽  
2019 ◽  
Vol 24 (10) ◽  
pp. 2020 ◽  
Author(s):  
Kiram Lee ◽  
Jin Choi ◽  
Bo Kyong Choi ◽  
Young-Mi Gu ◽  
Hyung Won Ryu ◽  
...  

Chronic obstructive pulmonary disease (COPD) is a major inflammatory lung disease characterized by irreversible and progressive airflow obstruction. Although corticosteroids are often used to reduce inflammation, steroid therapies are insufficient in patients with refractory COPD. Both serum amyloid A (SAA) and IL-33 have been implicated in the pathology of steroid-resistant lung inflammation. Picroside II isolated from Pseudolysimachion rotundum var. subintegrum (Plantaginaceae) is a major bioactive component of YPL-001, which has completed phase-2a clinical trials in chronic obstructive pulmonary disease patients. In this study, we investigated whether picroside II is effective in treating steroid refractory lung inflammation via the inhibition of the SAA-IL-33 axis. Picroside II inhibited LPS-induced SAA1 expression in human monocytes, which are resistant to steroids. SAA induced the secretion of IL-33 without involving cell necrosis. Picroside II, but not dexamethasone effectively inhibited SAA-induced IL-33 expression and secretion. The inhibitory effect by picroside II was mediated by suppressing the mitogen-activated protein kinase (MAPK) p38, ERK1/2, and nuclear factor-κB pathways. Our results suggest that picroside II negatively modulates the SAA-IL-33 axis that has been implicated in steroid-resistant lung inflammation. These findings provide valuable information for the development of picroside II as an alternative therapeutic agent against steroid refractory lung inflammation in COPD.


2014 ◽  
Vol 11 (Supplement 1) ◽  
pp. S76-S77 ◽  
Author(s):  
Alleluiah Rutebemberwa ◽  
Mark Stevens ◽  
Mario Perez ◽  
Lynelle Smith ◽  
Linda Sanders ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Hyojung Lee ◽  
Youngeun Kim ◽  
Hye Jin Kim ◽  
Soojin Park ◽  
Young Pyo Jang ◽  
...  

Chronic obstructive pulmonary disease (COPD), which is characterized by airway obstruction, leads to, as the two major forms of COPD, chronic bronchitis and emphysema. This study was conducted to evaluate the effects of herbal formula, PM014, in a murine model of COPD. Balb/c mice were treated once with each herb extract in PM014 or PM014 mixture via an oral injection. Lipopolysaccharide (LPS) or elastase/LPS were administrated to the mice to induce a disease that resembles COPD. PM014 treatment significantly attenuated the increased accumulation of immune cells in bronchoalveolar lavage fluid (BALF) compared to control mice. In addition, the TNF-αand IL-6 levels in BALF were decreased in the PM014 mice. Furthermore, histological analysis demonstrated that PM014 attenuated the hazardous effects of lung inflammation. These data suggest that PM014 exerts beneficial effects against forms of COPD such as lung inflammation.


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