scholarly journals Elevated GDF-15 contributes to pulmonary inflammation upon cigarette smoke exposure

2017 ◽  
Vol 10 (6) ◽  
pp. 1400-1411 ◽  
Author(s):  
F M Verhamme ◽  
L J M Seys ◽  
E G De Smet ◽  
S Provoost ◽  
W Janssens ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Pulmonary Inflammation ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure

Clarithromycin ameliorates pulmonary inflammation induced by short term cigarette smoke exposure in mice

2015 ◽  
Vol 35 ◽  
pp. 60-66 ◽  
Author(s):  
Masuo Nakamura ◽  
Hiroo Wada ◽  
Kojiro Honda ◽  
Keitaro Nakamoto ◽  
Toshiya Inui ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Pulmonary Inflammation ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Short Term

scholarly journals Pneumocystis murina Infection and Cigarette Smoke Exposure Interact To Cause Increased Organism Burden, Development of Airspace Enlargement, and Pulmonary Inflammation in Mice

2008 ◽  
Vol 76 (8) ◽  
pp. 3481-3490 ◽  
Author(s):  
Paul J. Christensen ◽  
Angela M. Preston ◽  
Tony Ling ◽  
Ming Du ◽  
W. Bradley Fields ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Pulmonary Inflammation ◽  
Airflow Obstruction ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Chronic Obstructive ◽  
Respiratory Pathogens ◽  
Obstructive Pulmonary Disease ◽  
Immunocompetent Mice

ABSTRACT Chronic obstructive pulmonary disease (COPD) is characterized by the presence of airflow obstruction and lung destruction with airspace enlargement. In addition to cigarette smoking, respiratory pathogens play a role in pathogenesis, but specific organisms are not always identified. Recent reports demonstrate associations between the detection of Pneumocystis jirovecii DNA in lung specimens or respiratory secretions and the presence of emphysema in COPD patients. Additionally, human immunodeficiency virus-infected individuals who smoke cigarettes develop early emphysema, but a role for P. jirovecii in pathogenesis remains speculative. We developed a new experimental model using immunocompetent mice to test the interaction of cigarette smoke exposure and environmentally acquired Pneumocystis murina infection in vivo. We hypothesized that cigarette smoke and P. murina would interact to cause increases in total lung capacity, airspace enlargement, and pulmonary inflammation. We found that exposure to cigarette smoke significantly increases the lung organism burden of P. murina. Pulmonary infection with P. murina, combined with cigarette smoke exposure, results in changes in pulmonary function and airspace enlargement characteristic of pulmonary emphysema. P. murina and cigarette smoke exposure interact to cause increased lung inflammatory cell accumulation. These findings establish a novel animal model system to explore the role of Pneumocystis species in the pathogenesis of COPD.

SHORT-TERM CIGARETTE SMOKE EXPOSURE POTENTIATES ENDOTOXIN-INDUCED PULMONARY INFLAMMATION

2007 ◽  
Vol 33 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Girish S. Kulkarni ◽  
Priya P. Nadkarni ◽  
Joseph M. Cerreta ◽  
Shuren Ma ◽  
Jerome O. Cantor
Keyword(s):  
Cigarette Smoke ◽  
Pulmonary Inflammation ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Short Term

scholarly journals Acute pulmonary inflammation is inhibited in CXCR3 knockout mice after short-term cigarette smoke exposure

2008 ◽  
Vol 29 (12) ◽  
pp. 1432-1439 ◽  
Author(s):  
Li Nie ◽  
Ruo-lan Xiang ◽  
Yong Liu ◽  
Wei-xun Zhou ◽  
Lei Jiang ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Knockout Mice ◽  
Pulmonary Inflammation ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Short Term

scholarly journals The Aryl Hydrocarbon Receptor Suppresses Chronic Smoke-Induced Pulmonary Inflammation

2021 ◽  
Vol 3 ◽  
Author(s):  
Necola Guerrina ◽  
Hussein Traboulsi ◽  
David H. Eidelman ◽  
Carolyn J. Baglole
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Cigarette Smoke ◽  
Therapeutic Potential ◽  
Pulmonary Inflammation ◽  
Giant Cells ◽  
Protective Role ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Aryl Hydrocarbon ◽  
Chronic Lung Diseases

The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor expressed in the lungs that is activated by numerous xenobiotic, endogenous and dietary ligands. Although historically the AhR is known for mediating the deleterious response to the environmental pollutant dioxin, emerging evidence supports a prominent role for the AhR in numerous biological process including inflammation. We have shown that the AhR suppresses pulmonary neutrophilia in response to acute cigarette smoke exposure. Whether the AhR can also prevent lung inflammation from chronic smoke exposure is not known but highly relevant, given that people smoke for decades. Using our preclinical smoke model, we report that exposure to chronic cigarette smoke for 8-weeks or 4 months significantly increased pulmonary inflammation, the response of which was greater in Ahr−/− mice. Notably, there was an increased number of multinucleated giant cells (MNGCs) in smoke-exposed Ahr−/− mice without a change in cytokine levels. These data support a protective role for the AhR against the deleterious effects of cigarette smoke, warranting continued investigation into its therapeutic potential for chronic lung diseases.

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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