scholarly journals Cigarette Smoke Particle-Induced Lung Injury and Iron Homeostasis

2022 ◽  
Vol Volume 17 ◽  
pp. 117-140
Author(s):  
Andrew J Ghio ◽  
Elizabeth N Pavlisko ◽  
Victor L Roggli ◽  
Nevins W Todd ◽  
Rahul G Sangani
Keyword(s):  
Lung Injury ◽  
Cigarette Smoke ◽  
Iron Homeostasis ◽  
Smoke Particle

scholarly journals Cigarette smoke exposure and alveolar macrophages: mechanisms for lung disease

Thorax ◽  
2021 ◽  
pp. thoraxjnl-2020-216296
Author(s):  
Sebastian T Lugg ◽  
Aaron Scott ◽  
Dhruv Parekh ◽  
Babu Naidu ◽  
David R Thickett
Keyword(s):  
Cigarette Smoking ◽  
Lung Injury ◽  
Lung Disease ◽  
Alveolar Macrophage ◽  
Cigarette Smoke ◽  
Alveolar Macrophages ◽  
Iron Homeostasis ◽  
Cigarette Smoke Exposure ◽  
Bacterial Killing ◽  
Macrophage Populations

Cigarette smoking is the leading cause of preventable death worldwide. It causes chronic lung disease and predisposes individuals to acute lung injury and pulmonary infection. Alveolar macrophages are sentinel cells strategically positioned in the interface between the airway lumen and the alveolar spaces. These are the most abundant immune cells and are the first line of defence against inhaled particulates and pathogens. Recently, there has been a better understanding about the ontogeny, phenotype and function of alveolar macrophages and their role, not only in phagocytosis, but also in initiating and resolving immune response. Many of the functions of the alveolar macrophage have been shown to be dysregulated following exposure to cigarette smoke. While the mechanisms for these changes remain poorly understood, they are important in the understanding of cigarette smoking-induced lung disease. We review the mechanisms by which smoking influences alveolar macrophage: (1) recruitment, (2) phenotype, (3) immune function (bacterial killing, phagocytosis, proteinase/anti-proteinase release and reactive oxygen species production) and (4) homeostasis (surfactant/lipid processing, iron homeostasis and efferocytosis). Further understanding of the mechanisms of cigarette smoking on alveolar macrophages and other lung monocyte/macrophage populations may allow novel ways of restoring cellular function in those patients who have stopped smoking in order to reduce the risk of subsequent infection or further lung injury.

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

scholarly journals p53- and PAI-1-mediated induction of C-X-C chemokines and CXCR2: importance in pulmonary inflammation due to cigarette smoke exposure

2016 ◽  
Vol 310 (6) ◽  
pp. L496-L506 ◽  
Author(s):  
Nivedita Tiwari ◽  
Amarnath S. Marudamuthu ◽  
Yoshikazu Tsukasaki ◽  
Mitsuo Ikebe ◽  
Jian Fu ◽  
...  
Keyword(s):  
Lung Injury ◽  
Cigarette Smoke ◽  
Lung Inflammation ◽  
Cellular Adhesion ◽  
Alveolar Epithelial Cells ◽  
Cigarette Smoke Exposure ◽  
Chronic Obstructive ◽  
P53 Expression ◽  
Cellular Adhesion Molecule ◽  
Pai 1

We previously demonstrated that tumor suppressor protein p53 augments plasminogen activator inhibitor-1 (PAI-1) expression in alveolar epithelial cells (AECs) during chronic cigarette smoke (CS) exposure-induced lung injury. Chronic lung inflammation with elevated p53 and PAI-1 expression in AECs and increased susceptibility to and exacerbation of respiratory infections are all associated with chronic obstructive pulmonary disease (COPD). We recently demonstrated that preventing p53 from binding to the endogenous PAI-1 mRNA in AECs by either suppressing p53 expression or blockading p53 interactions with the PAI-1 mRNA mitigates apoptosis and lung injury. Within this context, we now show increased expression of the C-X-C chemokines (CXCL1 and CXCL2) and their receptor CXCR2, and the intercellular cellular adhesion molecule-1 (ICAM-1), in the lung tissues of patients with COPD. We also found a similar increase in lung tissues and AECs from wild-type (WT) mice exposed to passive CS for 20 wk and in primary AECs treated with CS extract in vitro. Interestingly, passive CS exposure of mice lacking either p53 or PAI-1 expression resisted an increase in CXCL1, CXCL2, CXCR2, and ICAM-1. Furthermore, inhibition of p53-mediated induction of PAI-1 expression by treatment of WT mice exposed to passive CS with caveolin-1 scaffolding domain peptide reduced CXCL1, CXCL2, and CXCR2 levels and lung inflammation. Our study reveals that p53-mediated induction of PAI-1 expression due to chronic CS exposure exacerbates lung inflammation through elaboration of CXCL1, CXCL2, and CXCR2. We further provide evidence that targeting this pathway mitigates lung injury associated with chronic CS exposure.

Gene silencing of receptor-interacting protein 2 protects against cigarette smoke-induced acute lung injury

2019 ◽  
Vol 139 ◽  
pp. 560-568 ◽  
Author(s):  
Jinrui Dong ◽  
Wupeng Liao ◽  
Lay Hong Tan ◽  
Amy Yong ◽  
Wen Yan Peh ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Gene Silencing ◽  
Cigarette Smoke ◽  
Interacting Protein

CRTH2 antagonist, CT‑133, effectively alleviates cigarette smoke-induced acute lung injury

Life Sciences ◽  
2019 ◽  
Vol 216 ◽  
pp. 156-167 ◽  
Author(s):  
Musaddique Hussain ◽  
Chengyun Xu ◽  
Minli Yao ◽  
Qin Zhang ◽  
Junsong Wu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Cigarette Smoke

scholarly journals Angiotensin receptor blockade attenuates cigarette smoke–induced lung injury and rescues lung architecture in mice

2012 ◽  
Vol 122 (1) ◽  
pp. 229-240 ◽  
Author(s):  
Megan Podowski ◽  
Carla Calvi ◽  
Shana Metzger ◽  
Kaori Misono ◽  
Hataya Poonyagariyagorn ◽  
...  
Keyword(s):  
Lung Injury ◽  
Cigarette Smoke ◽  
Receptor Blockade ◽  
Angiotensin Receptor ◽  
Angiotensin Receptor Blockade

Effects of Eucalyptol in respiratory system mechanics on acute lung injury after exposure to short-term cigarette smoke

2019 ◽  
Vol 266 ◽  
pp. 33-38 ◽  
Author(s):  
Fladimir de Lima Gondim ◽  
Daniel Silveira Serra ◽  
Francisco Sales Ávila Cavalcante
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Cigarette Smoke ◽  
Respiratory System ◽  
Short Term ◽  
Respiratory System Mechanics

Apple polyphenol protects against cigarette smoke-induced acute lung injury

Nutrition ◽  
2013 ◽  
Vol 29 (1) ◽  
pp. 235-243 ◽  
Author(s):  
Meng-Jing Bao ◽  
Jian Shen ◽  
Yong-Liang Jia ◽  
Fen-Fen Li ◽  
Wen-Jiang Ma ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Cigarette Smoke
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