scholarly journals Dual interleukin-17A/F deficiency protects against acute and chronic response to cigarette smoke exposure in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hiroo Wada ◽  
Masuo Nakamura ◽  
Shin-Ichi Inoue ◽  
Akihiko Kudo ◽  
Tomoko Hanawa ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Cigarette Smoke ◽  
Inflammatory Responses ◽  
Inflammatory Cells ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Inflammatory Protein ◽  
Interleukin 17A ◽  
Macrophage Colony ◽  
Environmental Air

AbstractIL-17A and IL-17F are both involved in the pathogenesis of neutrophilic inflammation observed in COPD and severe asthma. To explore this, mice deficient in both Il17a and Il17f and wild type (WT) mice were exposed to cigarette smoke or environmental air for 5 to 28 days and changes in inflammatory cells in bronchoalveolar lavage (BAL) fluid were determined. We also measured the mRNA expression of keratinocyte derived chemokine (Kc), macrophage inflammatory protein-2 (Mip2), granulocyte–macrophage colony stimulating factor (Gmcsf) and matrix metalloproteinase-9 (Mmp9 ) in lung tissue after 8 days, and lung morphometric changes after 24 weeks of exposure to cigarette smoke compared to air-exposed control animals. Macrophage counts in BAL fluid initially peaked at day 8 and again on day 28, while neutrophil counts peaked between day 8 and 12 in WT mice. Mice dual deficient with Il17a and 1l17f showed similar kinetics with macrophages and neutrophils, but cell numbers at day 8 and mRNA expression of Kc, Gmcsf and Mmp9 were significantly reduced. Furthermore, airspaces in WT mice became larger after cigarette smoke exposure for 24 weeks, whereas this was not seen dual Il17a and 1l17f deficient mice. Combined Il17a and Il17f deficiency resulted in significant attenuation of neutrophilic inflammatory response and protection against structural lung changes after long term cigarette smoke exposure compared with WT mice. Dual IL-17A/F signalling plays an important role in pro-inflammatory responses associated with histological changes induced by cigarette smoke exposure.

scholarly journals Effect of Simvastatin on 5-HT and 5-HTT in a Rat Model of Pulmonary Artery Hypertension

2015 ◽  
Vol 37 (5) ◽  
pp. 1712-1724 ◽  
Author(s):  
Xue Jiang ◽  
LinDong Yuan ◽  
Peng Li ◽  
Jia Wang ◽  
Pengyu Wang ◽  
...  
Keyword(s):  
Body Weight ◽  
Pulmonary Artery ◽  
Cigarette Smoke ◽  
Rat Model ◽  
Structural Damage ◽  
Inflammatory Cells ◽  
Pulmonary Artery Hypertension ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Mean Pulmonary Arterial Pressure

Background/Aims: To investigaterole of serotonin (5-HT) and serotonin transporter (5-HTT) in a rat model of cigarette smoke-induced pulmonary artery hypertension (PAH) and the effect of statins on regulating 5HT and 5-HTT. Methods: A rat model of COPD comorbid with PAH was established by cigarette smoke exposure with or without simvastatin administration. The smoking and the simvastatin plus smoking groups were exposed to cigarette smoke daily, and the latter received simvastatin at 5mg/kg, once a day. After 16 weeks of cigarette smoke exposure, body weight and mean pulmonary arterial pressure (mPAP) were measured, bronchoalveolar lavage (BAL) was performed, and lung tissues and blood samples were collected to determine cardiopulmonary pathology, physiological indices, blood levelof 5-HT and expression of 5-HTT in the lung. Results: In addition to alveolar structural damage (COPD-like injury), chronic cigarette smoke exposure lead to pulmonary artery remodeling and PAH as evidenced by significant elevation of mPAP, RVHI, WT%and WA%. Cigarette smoke exposure resulted in significant reduction in animal body weight, and simvastatin significantly prevented smoke-induced weight loss. The number of inflammatory cells in BALF was dramatically increased in smoke exposed rats, and simvastatin dampened the number of leukocytes, neutrophils, lymphocytes, and macrophages. In addition, circulating 5-HTand expression of 5-HTT in the lung were significantly increased in the smoked rats compared to control rats, and it was significantly reduced by simvastatin. Alteration of BALF inflammatory cells, 5-HT and 5-HTT was significantly correlated with changes of mPAP, RVHI, WT% and WA%. Conclusions: Cigarette smoke exposure could result in not only COPD, but also PAH, which may attribute to the alteration of blood 5-HT and lung tissue 5-HTT. Simvastatin could significantly inhibited 5-HT and 5-HTT expression, and by which mechanism, it may protect animals from development of PAH.

scholarly journals Cigarette Smoke Specifically Affects Small Airway Epithelial Cell Populations and Triggers the Expansion of Inflammatory and Squamous Differentiation Associated Basal Cells

2021 ◽  
Vol 22 (14) ◽  
pp. 7646
Author(s):  
Christian T. Wohnhaas ◽  
Julia A. Gindele ◽  
Tobias Kiechle ◽  
Yang Shen ◽  
Germán G. Leparc ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Basal Cell ◽  
Secretory Cell ◽  
Inflammatory Responses ◽  
Airway Epithelial Cells ◽  
Smoke Exposure ◽  
Small Airway ◽  
Cigarette Smoke Exposure ◽  
Small Airways ◽  
Airway Epithelial

Smoking is a major risk factor for chronic obstructive pulmonary disease (COPD) and causes remodeling of the small airways. However, the exact smoke-induced effects on the different types of small airway epithelial cells (SAECs) are poorly understood. Here, using air–liquid interface (ALI) cultures, single-cell RNA-sequencing reveals previously unrecognized transcriptional heterogeneity within the small airway epithelium and cell type-specific effects upon acute and chronic cigarette smoke exposure. Smoke triggers detoxification and inflammatory responses and aberrantly activates and alters basal cell differentiation. This results in an increase of inflammatory basal-to-secretory cell intermediates and, particularly after chronic smoke exposure, a massive expansion of a rare inflammatory and squamous metaplasia associated KRT6A+ basal cell state and an altered secretory cell landscape. ALI cultures originating from healthy non-smokers and COPD smokers show similar responses to cigarette smoke exposure, although an increased pro-inflammatory profile is conserved in the latter. Taken together, the in vitro models provide high-resolution insights into the smoke-induced remodeling of the small airways resembling the pathological processes in COPD airways. The data may also help to better understand other lung diseases including COVID-19, as the data reflect the smoke-dependent variable induction of SARS-CoV-2 entry factors across SAEC populations.

scholarly journals Protective Effects of Quercetin on Livers from Mice Exposed to Long-Term Cigarette Smoke

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Pedro A. Machado-Junior ◽  
Natália P. S. Araújo ◽  
Ana B. F. Souza ◽  
Thalles F. Castro ◽  
Michel Oliveira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Cigarette Smoke ◽  
Liver Diseases ◽  
Inflammatory Cells ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Protective Effects ◽  
Histopathological Changes

Cigarette smoke is highly toxic, and it can promote increased production of reactive species and inflammatory response and leads to liver diseases. Quercetin is a flavonoid that displays antioxidant and anti-inflammatory activities in liver diseases. This study aimed at evaluating the protective effects of quercetin on livers from mice exposed to long-term cigarette smoke exposure. Male C57BL/6 mice were divided into five groups: control (CG), vehicle (VG), quercetin (QG), cigarette smoke (CSG), quercetin, and cigarette smoke (QCSG). CSG and QCSG were exposed to cigarette smoke for sixty consecutive days; at the end of the exposures, all animals were euthanized. Mice that received quercetin daily and were exposed to cigarette smoke showed a reduced influx of inflammatory cells, oxidative stress, inflammatory reaction, and histopathological changes in the liver, compared to CSG. These results suggest that quercetin may be an effective adjuvant for treating damage to the liver due to 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
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