Cigarette smoke exposure potentiates bleomycin-induced lung fibrosis in guinea pigs

2003 ◽  
Vol 285 (4) ◽  
pp. L949-L956 ◽  
Author(s):  
José Cisneros-Lira ◽  
Miguel Gaxiola ◽  
Carlos Ramos ◽  
Moisés Selman ◽  
Annie Pardo
Keyword(s):  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Guinea Pigs ◽  
Lung Fibrosis ◽  
Smooth Muscle Actin ◽  
Smoke Exposure ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Tobacco Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Fibroblast Proliferation

The role of tobacco smoking in the development and outcome of pulmonary fibrosis is uncertain. To approach the effects of cigarette smoke on bleomycin-induced lung fibrosis, we studied five groups of guinea pigs: 1) controls, 2) instilled with bleomycin (B), 3) exposed to tobacco smoke for 6 wk (TS), 4) bleomycin instillation plus tobacco smoke exposure for 6 wk (B+TS), and 5) tobacco smoke exposure for 6 wk and bleomycin after smoking (TS/B). Guinea pigs receiving bleomycin and tobacco smoke exposure exhibited higher fibrotic lesions including a significant increase in the number of positive α-smooth muscle actin cells compared with bleomycin alone (B+TS, 3.4 ± 1.2%; TS/B, 3.7 ± 1.5%; B, 2.3 ± 1.5%; P < 0.01). However, only the TS/B group reached a significant increase in lung collagen compared with the bleomycin group (TS/B, 3.5 ± 0.7; B ± TS, 2.9 ± 0.4; B, 2.4 ± 0.2 mg hydroxyproline/lung; P < 0.01). Bronchoalveolar lavage (BAL) from TS/B showed an increased number of eosinophils and higher levels of IL-4 and tissue inhibitor of metalloproteinase-2 ( P < 0.01 for all comparisons) and induced a significant increase in fibroblast proliferation ( P < 0.05). Importantly, smoke exposure alone induced an increase in BAL neutrophils, matrix metalloproteinase-9, and fibroblast proliferation compared with controls, suggesting that tobacco smoke creates a profibrotic milieu that may contribute to the increased bleomycin-induced fibrosis.

Comparison of Oxidative Effects of Electronic Cigarette and Tobacco Smoke Exposure Performed Experimentally

2021 ◽  
pp. 1-7
Author(s):  
Oktay Aslaner
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Smoke Exposure ◽  
Electronic Cigarette ◽  
Tobacco Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Exposure Group ◽  
Oxidative Effects

<b><i>Objective:</i></b> Cigarette smoking is a life-threatening habit that has rapidly spread in every socioeconomic part of the public worldwide. There exist mechanisms of nicotine delivery available to use in the hope of halting cigarette smoking, and the electronic cigarette (EC) is one of the common methods used for tobacco smoking replacement. This study aimed to investigate experimentally the oxidative effects of tobacco smoke and EC smoke which contain nicotine. <b><i>Method:</i></b> We constructed smoke circuit rooms for exposing the rats to EC or tobacco smoke. Three groups were created, the control group (<i>N</i> = 8); the electronic cigarette group (<i>N</i> = 8), exposure to electronic cigarette smoke for 2 h per day; and the tobacco group (<i>N</i> = 8), exposure to traditional cigarette smoke for 2 h per day. After the first and second week of exposure, blood samples were obtained, and serum oxidative stress index (OSI), paraoxonase 1 (PON1) activity, and prolidase levels were evaluated. <b><i>Results:</i></b> Higher values of OSI and prolidase levels were detected in the first week of EC or tobacco smoke exposure in both study groups (<i>p</i> &#x3c; 0.001) when compared with the control group, and partial decrements were observed in the second week. By contrast, elevated PON1 levels were observed in the second week after EC or tobacco smoke exposure. The highest OSI levels were observed in the tobacco smoke group (<i>p</i> &#x3c; 0.001). The lowest values of PON1 levels were detected in the first week of the electronic cigarette smoke group, and this decremental value was statistically different than normal, the second week of the electronic cigarette smoke group, the first week of the traditional cigarette smoke exposure group, and the second week of the traditional cigarette smoke exposure group values (<i>p</i> &#x3c; 0.000). <b><i>Conclusion:</i></b> Our results indicate that EC smoke induced oxidative stress. Therefore, ECs are potentially risky for human health and can lead to important health problems.

Cigarette Smoke Exposure and Acute Respiratory Infection in Children Under Five: A Meta-Analysis

2020 ◽  
Author(s):  
Maya Ayu Riestiyowati ◽  
◽  
Setyo Sri Rahardjo ◽  
Vitri Widyaningsih ◽  
◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Respiratory Infection ◽  
Tobacco Smoke ◽  
Acute Respiratory Infection ◽  
Meta Analysis ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Children Under Five ◽  
Under Five

Background: Acute Respiratory Infections are classified into the upper and lower respiratory tract infections, contributing to the leading cause of death among children under five globally. The estimation showed the deaths of more than 800,000 children under five every year or about 2,200 per day. One of the risk factors for ARI in children under five years of age is secondary exposure to tobacco smoke. This study aimed to examine the effect of cigarette smoke exposure and acute respiratory infection in children under five. Subjects and Method: This was meta analysis and systematic review. The study was conducted by collecting published articles from Google Scholar, Pubmed, and Springer Link databases, from year 2010 to 2019. Keywords used “risk factor” OR “passive smoking” OR “secondhand smoking” AND “ARI due to children under five”. The inclusion criteria were full text, using English language, using cross-sectional study design, and reporting adjusted odds ratio. The collected articles were selected by PRISMA flow chart. The quantitative data were analyzed by fixed effect model using Revman 5.3. Results: 6 studies from Cameroon, Ethiopia, India, Nepal, and Nigeria reported that tobacco smoke exposure increased the risk of acute respiratory infection in children under five (aOR=1.39; 95% CI= 1.22 to 1.58; p<0.001). Conclusion: Tobacco smoke exposure increases the risk of acute respiratory infection in children under five. Keywords: tobacco smoke, acute respiratory infection, children under five Correspondence: Maya Ayu Riestiyowati. Masters Program in Public Health. Universitas Sebelas Maret, Jl. Ir. Sutami 36A, Surakarta 57126, Central Java. Email: [email protected]. Mobile: 081235840067.

Respiratory epithelial permeability after cigarette smoke exposure in guinea pigs

1989 ◽  
Vol 66 (5) ◽  
pp. 2109-2116 ◽  
Author(s):  
A. R. Burns ◽  
S. P. Hosford ◽  
L. A. Dunn ◽  
D. C. Walker ◽  
J. C. Hogg
Keyword(s):  
Cigarette Smoke ◽  
Guinea Pigs ◽  
Alveolar Epithelium ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Gel Chromatography ◽  
Type I ◽  
Electron Microscopic ◽  
Type I Cells ◽  
I Cells

The purpose of this study was to determine the pathology of cigarette smoke-increased permeability at the bronchioalveolar junction of the guinea pig. After exposure to either smoke or room air, guinea pigs were anesthetized and fluorescein isothiocyanate-dextran (FITC-D, mol wt 10,000) was aerosolized into their lungs. Blood samples taken through a carotid arterial cannula were analyzed by gel chromatography and spectrofluorometry for the presence of FITC-D. The results confirmed that, after smoke exposure, increased amounts of intact FITC-D molecules with a reported Einstein-Stokes radius of 22.2 A crossed the respiratory epithelium into the vascular space. Transmission electron-microscopic studies showed that the FITC-D diffused across damaged type I pneumocyte membranes and cytoplasm to reach the basal lamina and entered the alveolar capillaries through endothelial tight junctions. Damage to the alveolar epithelium was more frequent for the smoke-exposed animals than the room air-exposed animals (P less than 0.05). We conclude that smoke exposure damages type I cells and that inhaled FITC-D crosses the epithelial barrier at damaged type I cells of the bronchioloalveolar junctions.

Cigarette smoke upregulates pulmonary vascular matrix metalloproteinases via TNF-α signaling

2007 ◽  
Vol 292 (1) ◽  
pp. L125-L133 ◽  
Author(s):  
J. L. Wright ◽  
H. Tai ◽  
R. Wang ◽  
X. Wang ◽  
A. Churg
Keyword(s):  
Pulmonary Hypertension ◽  
Matrix Metalloproteinases ◽  
Cigarette Smoke ◽  
Vascular Remodeling ◽  
Smoke Exposure ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Cigarette Smoke Exposure ◽  
Mrna Levels ◽  
Gelatinase Activity ◽  
Tnf Α

Cigarette smoke exposure causes vascular remodeling and pulmonary hypertension by poorly understood mechanisms. To ascertain whether cigarette smoke exposure affects production of matrix metalloproteinases (MMPs) in the pulmonary vessels, we exposed C57Bl/6 (C57) mice or mice lacking TNF-α receptors (TNFRKO) to smoke daily for 2 wk or 6 mo. Using laser capture microdissection and RT-PCR analysis, we examined gene expression of MMP-2, MMP-9, MMP-12, MMP-13, and tissue inhibitor of metalloproteinase (TIMP-1) and examined protein production by immunohistochemistry for MMP-2, MMP-9, and MMP-12 in small intrapulmonary arteries. At 2 wk, mRNA levels of TIMP-1 and all MMPs were increased in the C57, but not TNFRKO, mice, and immunoreactive protein for MMP-2, MMP-9, and MMP-12 was also increased in the C57 mice. Increased gelatinase activity was identified by in situ and bulk tissue zymography. At 6 mo, only MMP-12 mRNA levels remained increased in the C57 mice, but at a much lower level; however, MMP-2 mRNA levels increased in the TNFRKO mice. We conclude that smoke exposure increases MMP production in the small intrapulmonary arteries but that, with the exception of MMP-12, increased MMP production is transient. MMPs probably play a role in smoke-induced vascular remodeling, as they do in other forms of pulmonary hypertension, implying that MMP inhibitors might be beneficial. MMP production is largely TNF-α dependent, further supporting the importance of TNF-α in the pathogenesis of cigarette smoke-induced lung disease.

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