scholarly journals The protective role of Zingerone in a murine asthma model via activation of the AMPK/Nrf2/HO-1 pathway

2020 ◽  
Author(s):  
Yingjie Zhu ◽  
Jingjing Luo ◽  
You Xu ◽  
Shucheng Hua ◽  
Dan Li ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Active Compound ◽  
Protective Role ◽  
Asthma Model ◽  
Common Illnesses ◽  
Murine Asthma Model ◽  
Chronic Airway

Asthma is one of the most common illnesses associated with chronic airway inflammation; however, there are currently no effective therapies apart from glucocorticoids. Zingerone (ZIN), an active compound isolated from...

scholarly journals Different role of CD30 in the development of acute and chronic airway inflammation in a murine asthma model

2009 ◽  
Vol 39 (7) ◽  
pp. 1736-1742 ◽  
Author(s):  
Tobias Polte ◽  
Lena Fuchs ◽  
Ann-Kathrin Behrendt ◽  
Gesine Hansen
Keyword(s):  
Airway Inflammation ◽  
Asthma Model ◽  
Murine Asthma Model ◽  
Chronic Airway

Regulation of Th17/Treg function contributes to the attenuation of chronic airway inflammation by icariin in ovalbumin-induced murine asthma model

Immunobiology ◽  
2015 ◽  
Vol 220 (6) ◽  
pp. 789-797 ◽  
Author(s):  
Ying Wei ◽  
Baojun Liu ◽  
Jing Sun ◽  
Yubao Lv ◽  
Qingli Luo ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Asthma Model ◽  
Treg Function ◽  
Murine Asthma Model ◽  
Chronic Airway

Astragalus membranaceus modulates Th1/2 immune balance and activates PPARγ in a murine asthma model

2014 ◽  
Vol 92 (5) ◽  
pp. 397-405 ◽  
Author(s):  
Shih-Ming Chen ◽  
Yau-Sheng Tsai ◽  
Su-Wen Lee ◽  
Ya-Hui Liu ◽  
Shuen-Kuei Liao ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Chinese Herb ◽  
A549 Cells ◽  
Nuclear Hormone Receptor ◽  
Astragalus Membranaceus ◽  
Luciferase Reporter ◽  
Mrna Levels ◽  
Th2 Cytokines ◽  
Asthma Model ◽  
Murine Asthma Model

Astragalus membranaceus, a traditional Chinese herb, has been used to improve airway inflammation and asthma. The present study investigated whether A. membranaceus has immunotherapeutic effects on asthma, a chronic inflammatory mucosal disease that is associated with excess production of IgE, eosinophilia, T helper 2 (Th2) cytokines, and bronchial hyperresponsiveness. An ovalbumin (OVA)-induced, chronic inflammatory airway murine asthma model was used to examine the status of pulmonary inflammation after the administration of A. membranaceus. The IgE levels in serum and bronchoalveolar lavage fluid showed a tendency to decrease after the administration of A. membranaceus. The number of eosinophils decreased and infiltration of inflammatory cells and collagen deposition declined in lung sections after A. membranaceus administration. The RNA and protein levels of Th2 cytokines and the ratio of the GATA3/T-bet mRNA levels decreased after A. membranaceus treatment. Furthermore, the mRNA level of peroxisome proliferator-activated receptor γ (PPARγ), a nuclear hormone receptor, increased in the lung tissues of A. membranaceus–treated mice. Finally, an A. membranaceus water extract activated PPARγ activity in either human embryonic kidney 293 (HEK293) or A549 cells in a PPARγ-responsive element-containing luciferase reporter assay. These results indicate that A. membranaceus has an inhibitory effect on airway inflammation in a murine model of asthma through modulating the imbalanced relationship between Th1 and Th2 cytokines.

scholarly journals Role of Neuro‐immune Interactions in a Cigarette Smoke‐induced Chronic Airway Inflammation Mouse Model

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Kata Csekő ◽  
István Szitter ◽  
Zsófia Hajna ◽  
Krisztián Elekes ◽  
Ágnes Kemény ◽  
...  
Keyword(s):  
Mouse Model ◽  
Airway Inflammation ◽  
Cigarette Smoke ◽  
Chronic Airway

RAGE mediates airway inflammation via the HDAC1 pathway in a toluene diisocyanate-induced murine asthma model

2020 ◽  
Author(s):  
Xianru Peng ◽  
Minyu Huang ◽  
Wenqu Zhao ◽  
Zihan Lan ◽  
Xiaohua Wang ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Histone Deacetylase ◽  
Toluene Diisocyanate ◽  
Epithelial Cell Line ◽  
Akt Inhibitor ◽  
Histone Deacetylase 1 ◽  
Asthma Model ◽  
Key Words Toluene ◽  
Murine Asthma Model

Abstract BackgroundExposure to toluene diisocyanate (TDI) is a significant pathogenic factor for asthma. We previously reported that receptor for advanced glycation end products (RAGE) plays a key role in TDI-induced asthma; however, the mechanism is not clear. Epigenetic alterations of histone deacetylase (HDAC) are associated with allergic asthma. However, its effect in TDI-induced asthma is not known. The purpose of this study was to determine the role of RAGE and HDAC1 in the regulation of airway inflammation using a TDI-induced asthma model.MethodsBALB/c mice were sensitized, and challenged by TDI to establish murine asthma models. FPS-ZM1 (RAGE inhibitor), JNJ-26482585 and romidepsin (HDAC inhibitor) were given intraperitoneally before each challenge. The human bronchial epithelial cell line 16HBE was stimulated by TDI-human serum albumin (TDI-HSA) in vitro. RAGE knockdown cells were constructed and evaluated, and MK2006 (AKT inhibitor) was used in in vitro experiments.ResultsIn the TDI-induced asthmatic mice, airway reactivity, the level of Th2 cytokines in lymph supernatant, IgE, airway inflammation, and goblet cell metaplasia were all significantly increased. The increases were suppressed by FPS-ZM1, JNJ-26482585, and romidepsin. The expression of HDAC1, RAGE, and p-AKT/t-AKT was also upregulated in TDI-induced asthmatic mice, and the expressions were attenuated by FPS-ZM1. Knockdown of RAGE attenuated the upregulation of HDAC1 and phospho-AKT (p-AKT) in 16HBE cells stimulated by TDI-HSA. Treatment with the AKT inhibitor MK2006 suppressed TDI-induced HDAC1 expression. ConclusionRAGE mediates airway inflammation in a TDI-induced murine asthma model, partly via the HDAC1 pathway. Key words: Toluene diisocyanate, asthma, histone deacetylase 1, advanced glycosylation end product receptor

scholarly journals HDAC2 attenuates airway inflammation by suppressing IL-17A production in HDM-challenged mice

2019 ◽  
Vol 316 (1) ◽  
pp. L269-L279 ◽  
Author(s):  
Tianwen Lai ◽  
Mindan Wu ◽  
Chao Zhang ◽  
Luanqing Che ◽  
Feng Xu ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Inflammatory Cytokines ◽  
Allergic Inflammation ◽  
Allergic Airway Inflammation ◽  
Inflammatory Cells ◽  
Protective Role ◽  
In Vivo Models

Histone deacetylase (HDAC)2 is expressed in airway epithelium and plays a pivotal role in inflammatory cells. However, the role of HDAC2 in allergic airway inflammation remains poorly understood. In the present study, we determined the role of HDAC2 in airway inflammation using in vivo models of house dust mite (HDM)-induced allergic inflammation and in vitro cultures of human bronchial epithelial (HBE) cells exposed to HDM, IL-17A, or both. We observed that HDM-challenged Hdac2+/− mice exhibited substantially enhanced infiltration of inflammatory cells. Higher levels of T helper 2 cytokines and IL-17A expression were found in lung tissues of HDM-challenged Hdac2+/− mice. Interestingly, IL-17A deletion or anti-IL-17A treatment reversed the enhanced airway inflammation induced by HDAC2 impairment. In vitro, HDM and IL-17A synergistically decreased HDAC2 expression in HBE cells. HDAC2 gene silencing further enhanced HDM- and/or IL-17A-induced inflammatory cytokines in HBE cells. HDAC2 overexpresion or blocking IL-17A gene expression restored the enhanced inflammatory cytokines. Collectively, these results support a protective role of HDAC2 in HDM-induced airway inflammation by suppressing IL-17A production and might suggest that activation of HDAC2 and/or inhibition of IL-17A production could prevent the development of allergic airway inflammation.

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