Smoking fruit flies – Impact of cigarette smoke exposure on the airway epithelium of Drosophila melanogaster

Pneumologie ◽  
2016 ◽  
Vol 70 (07) ◽  
Author(s):  
A Bhandari ◽  
T Roeder ◽  
J Erdmann
Keyword(s):  
Drosophila Melanogaster ◽  
Cigarette Smoke ◽  
Airway Epithelium ◽  
Fruit Flies ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure

Cigarette smoke exposure induces substantial changes in the airway epithelium of a Drosophila COPD model

Pneumologie ◽  
2016 ◽  
Vol 70 (07) ◽  
Author(s):  
M Thiedmann ◽  
R Prange ◽  
A Bhandari ◽  
K Kallsen ◽  
C Fink ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Airway Epithelium ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure

scholarly journals Macrophages Inhibit Ciliary Protein Levels by Secreting BMP-2 Leading to Airway Epithelial Remodeling Under Cigarette Smoke Exposure

2021 ◽  
Vol 8 ◽  
Author(s):  
Zhigang Wang ◽  
Wenzhang Liang ◽  
Cuiqing Ma ◽  
Jiachao Wang ◽  
Xue Gao ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Airway Epithelium ◽  
Airway Remodeling ◽  
Inhibitory Effect ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Protein Levels ◽  
Ciliary Protein ◽  
Β Tubulin ◽  
Stimulation Of

Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease with high morbidity and mortality worldwide. So far, smoking is still its leading cause. The characteristics of COPD are emphysema and airway remodeling, as well as chronic inflammation, which were predominated by macrophages. Some studies have reported that macrophages were involved in emphysema and chronic inflammation, but whether there is a link between airway remodeling and macrophages remains unclear. In this study, we found that both acute and chronic cigarette smoke exposure led to an increase of macrophages in the lung and a decrease of ciliated cells in the airway epithelium of a mouse model. The results of in vitro experiments showed that the ciliary protein (β-tubulin-IV) levels of BEAS-2B cells could be inhibited when co-cultured with human macrophage line THP-1, and the inhibitory effect was augmented with the stimulation of cigarette smoke extract (CSE). Based on the results of transcriptome sequencing, we focused on the protein, bone morphogenetic protein-2 (BMP-2), secreted by the macrophage, which might mediate this inhibitory effect. Further studies confirmed that BMP-2 protein inhibited β-tubulin-IV protein levels of BEAS-2B cells under the stimulation of CSE. Coincidentally, this inhibitory effect could be nearly blocked by the BMP receptor inhibitor, LDN, or could be interfered with BMP-2 siRNA. This study suggests that activation and infiltration of macrophages in the lung induced by smoke exposure lead to a high expression of BMP-2, which in turn inhibits the ciliary protein levels of the bronchial epithelial cells, contributing to the remodeling of airway epithelium, and aggravates the development of COPD.

Differential effects of dexamethasone and roflumilast on asthma in mice with or without short cigarette smoke exposure

2021 ◽  
pp. 102052
Author(s):  
Junichiro Kawagoe ◽  
Maeda Yuki ◽  
Ryota Kikuchi ◽  
Maki Takahashi ◽  
Jun-ichi Fuchikami ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Differential Effects

scholarly journals Cigarette Smoke Exposure Worsens Endotoxin-Induced Lung Injury and Pulmonary Edema in Mice

2017 ◽  
Vol 19 (9) ◽  
pp. 1033-1039 ◽  
Author(s):  
Jeffrey E Gotts ◽  
Jason Abbott ◽  
Xiaohui Fang ◽  
Haru Yanagisawa ◽  
Naoki Takasaka ◽  
...  
Keyword(s):  
Lung Injury ◽  
Pulmonary Edema ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure
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