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1.
PLoS One ; 19(4): e0301515, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38557563

RESUMO

INTRODUCTION: Results of the impact of lockdowns and stay-at-home orders during the COVID-19 pandemic on changes in cigarette smoking are mixed. Previous studies examining smoking changes during the early stages of the pandemic in 2020 have mainly focused on smoker's perception of changes in cigarette consumption. Such measure has not been widely used in other contexts, and therefore we aim to compare the discrepancy between smokers' perceived changes in cigarette smoking and the actual change in the number of cigarettes smoked, using repeated measurements. METHODS: We included 134 smokers from the French TEMPO cohort with repeated measurements of their perceived changes in smoking habits during the first phase of the COVID-19 pandemic and the number of cigarettes smoked repeatedly from March to May 2020. We used generalized estimation equations (GEE) to examine the association between changes in the number of cigarettes smoked and the odds of mismatched answers. RESULTS: The results suggest that at each study wave, 27-45% of participants provided mismatching answers between their perceived change in smoking habits and the actual change in the number of cigarettes smoked daily, measured repeatedly. Results from GEE analysis demonstrated that a mismatching assessment of smoking behavior was elevated among those who had an increase (OR = 2.52 [1.37;4.65]) or a decrease (OR = 5.73 [3.27;10.03]) in number of cigarettes smoked. DISCUSSION: Our findings highlight the possibility of obtaining different results depending on how changes in tobacco smoking are measured. This highlights the risk of underestimating the actual changes in cigarette smoking during the COVID-19 pandemic, but also more generally when validating public health interventions or smoking cessation programs. Therefore, objective measures such as the actual consumption of psychoactive substances should be utilized, preferably on a longitudinal basis, to mitigate recall bias.


Assuntos
COVID-19 , Fumar Cigarros , Humanos , Estudos Longitudinais , Pandemias , Fumar Cigarros/epidemiologia , COVID-19/epidemiologia , Percepção
3.
Respir Res ; 25(1): 158, 2024 Apr 09.
Artigo em Inglês | MEDLINE | ID: mdl-38594707

RESUMO

BACKGROUND: Airway remodelling plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Epithelial-mesenchymal transition (EMT) is a significant process during the occurrence of airway remodelling. Increasing evidence suggests that glucose transporter 3 (GLUT3) is involved in the epithelial mesenchymal transition (EMT) process of various diseases. However, the role of GLUT3 in EMT in the airway epithelial cells of COPD patients remains unclear. METHODS: We detected the levels of GLUT3 in the peripheral lung tissue of COPD patients and cigarette smoke (CS)-exposed mice. Two Gene Expression Omnibus GEO datasets were utilised to analyse GLUT3 gene expression profiles in COPD. Western blot and immunofluorescence were used to detect GLUT3 expression. In addition, we used the AAV9-GLUT3 inhibitor to reduce GLUT3 expression in the mice model. Masson's staining and lung function measurement were used detect the collagen deposition and penh in the mice. A cell study was performed to confirm the regulatory effect of GLUT3. Inhibition of GLUT3 expression with siRNA, Western blot, and immunofluorescence were used to detect the expression of E-cadherin, N-cadherin, vimentin, p65, and ZEB1. RESULTS: Based on the GEO data set analysis, GLUT3 expression in COPD patients was higher than in non-smokers. Moreover, GLUT3 was highly expressed in COPD patients, CS exposed mice, and BEAS-2B cells treated with CS extract (CSE). Further research revealed that down-regulation of GLUT3 significantly alleviated airway remodelling in vivo and in vitro. Lung function measurement showed that GLUT3 reduction reduced airway resistance in experimental COPD mice. Mechanistically, our study showed that reduction of GLUT3 inhibited CSE-induced EMT by down-regulating the NF-κB/ZEB1 pathway. CONCLUSION: We demonstrate that CS enhances the expression of GLUT3 in COPD and further confirm that GLUT3 may regulate airway remodelling in COPD through the NF-κB/ZEB1 pathway; these findings have potential value in the diagnosis and treatment of COPD. The down-regulation of GLUT3 significantly alleviated airway remodelling and reduced airway resistance in vivo. Our observations uncover a key role of GLUT3 in modulating airway remodelling and shed light on the development of GLUT3-targeted therapeutics for COPD.


Assuntos
Fumar Cigarros , Doença Pulmonar Obstrutiva Crônica , Humanos , Camundongos , Animais , NF-kappa B/metabolismo , Remodelação das Vias Aéreas , Fumar Cigarros/efeitos adversos , Transportador de Glucose Tipo 3/metabolismo , Doença Pulmonar Obstrutiva Crônica/metabolismo , Transição Epitelial-Mesenquimal , Células Epiteliais/metabolismo , Homeobox 1 de Ligação a E-box em Dedo de Zinco/genética
4.
Am J Hum Genet ; 111(4): 636-653, 2024 Apr 04.
Artigo em Inglês | MEDLINE | ID: mdl-38490207

RESUMO

Cigarette smoking adversely affects many aspects of human health, and epigenetic responses to smoking may reflect mechanisms that mediate or defend against these effects. Prior studies of smoking and DNA methylation (DNAm), typically measured in leukocytes, have identified numerous smoking-associated regions (e.g., AHRR). To identify smoking-associated DNAm features in typically inaccessible tissues, we generated array-based DNAm data for 916 tissue samples from the GTEx (Genotype-Tissue Expression) project representing 9 tissue types (lung, colon, ovary, prostate, blood, breast, testis, kidney, and muscle). We identified 6,350 smoking-associated CpGs in lung tissue (n = 212) and 2,735 in colon tissue (n = 210), most not reported previously. For all 7 other tissue types (sample sizes 38-153), no clear associations were observed (false discovery rate 0.05), but some tissues showed enrichment for smoking-associated CpGs reported previously. For 1,646 loci (in lung) and 22 (in colon), smoking was associated with both DNAm and local gene expression. For loci detected in both lung and colon (e.g., AHRR, CYP1B1, CYP1A1), top CpGs often differed between tissues, but similar clusters of hyper- or hypomethylated CpGs were observed, with hypomethylation at regulatory elements corresponding to increased expression. For lung tissue, 17 hallmark gene sets were enriched for smoking-associated CpGs, including xenobiotic- and cancer-related gene sets. At least four smoking-associated regions in lung were impacted by lung methylation quantitative trait loci (QTLs) that co-localize with genome-wide association study (GWAS) signals for lung function (FEV1/FVC), suggesting epigenetic alterations can mediate the effects of smoking on lung health. Our multi-tissue approach has identified smoking-associated regions in disease-relevant tissues, including effects that are shared across tissue types.


Assuntos
Fumar Cigarros , Metilação de DNA , Masculino , Feminino , Humanos , Metilação de DNA/genética , Epigênese Genética , Estudo de Associação Genômica Ampla , Fumar/efeitos adversos , Fumar/genética , Expressão Gênica
5.
Respir Res ; 25(1): 148, 2024 Mar 30.
Artigo em Inglês | MEDLINE | ID: mdl-38555458

RESUMO

BACKGROUND: Astaxanthin (AXT) is a keto-carotenoid with a variety of biological functions, including antioxidant and antifibrotic effects. Small airway remodeling is the main pathology of chronic obstructive pulmonary disease (COPD) and is caused by epithelial-to-mesenchymal transition (EMT) and fibroblast differentiation and proliferation. Effective therapies are still lacking. This study aimed to investigate the role of AXT in small airway remodeling in COPD and its underlying mechanisms. METHODS: First, the model of COPD mice was established by cigarette smoke (CS) exposure combined with intraperitoneal injection of cigarette smoke extract (CSE). The effects of AXT on the morphology of CS combined with CSE -induced emphysema, EMT, and small airway remodeling by using Hematoxylin-eosin (H&E) staining, immunohistochemical staining, and western blot. In addition, in vitro experiments, the effects of AXT on CSE induced-EMT and fibroblast function were further explored. Next, to explore the specific mechanisms underlying the protective effects of AXT in COPD, potential targets of AXT in COPD were analyzed using network pharmacology. Finally, the possible mechanism was verified through molecular docking and in vitro experiments. RESULTS: AXT alleviated pulmonary emphysema, EMT, and small airway remodeling in a CS combined with CSE -induced mouse model. In addition, AXT inhibited the EMT process in airway cells and the differentiation and proliferation of fibroblasts. Mechanistically, AXT inhibited myofibroblast activation by directly binding to and suppressing the phosphorylation of AKT1. Therefore, our results show that AXT protects against small airway remodeling by inhibiting AKT1. CONCLUSIONS: The present study identified and illustrated a new food function of AXT, indicating that AXT could be used in the therapy of COPD-induced small airway remodeling.


Assuntos
Fumar Cigarros , Doença Pulmonar Obstrutiva Crônica , Enfisema Pulmonar , Camundongos , Animais , Fumar Cigarros/efeitos adversos , Remodelação das Vias Aéreas , Simulação de Acoplamento Molecular , Transdução de Sinais , Doença Pulmonar Obstrutiva Crônica/metabolismo , Enfisema Pulmonar/induzido quimicamente , Enfisema Pulmonar/tratamento farmacológico , Xantofilas
6.
Anal Chim Acta ; 1300: 342446, 2024 Apr 29.
Artigo em Inglês | MEDLINE | ID: mdl-38521574

RESUMO

BACKGROUND: In vitro toxicity assessment studies with various experimental models and exposure modalities frequently generate diverse outcomes. In the prevalent experimental, aerosol pollutants are dissolved in culture medium through capture for exposure to two-dimensional planar cellular models in multiwell plates via immersion. However, this approach can generate restricted and inconclusive experimental data, significantly constraining the applicability of risk assessment outcomes. Herein, the in vitro cocultivation of lung epithelial and/or vascular endothelial cells was performed using self-designed bionic-lung microfluidic chip housing a gas-concentration gradient generator (GCGG) unit. Exposure experiments involving a concentration gradient of cigarette smoke (CS) aerosol were then conducted through an original assembled real-time aerosol exposure system. RESULTS: Transcriptomic analysis revealed a potential involvement of the cGMP-signaling pathway following online CS aerosol exposure on different cell culture models. Furthermore, distinct responses to different concentrations of CS aerosol exposure on different culture models were highlighted by detecting inflammation- and oxidative stress-related biomarkers (i.e., cell viability, reactive oxygen species, nitric oxide, IL-6, IL-8, TNF-α, GM-CSF, malondialdehyde, and superoxide dismutase). SIGNIFICANT: The results underscore the importance of improving chip biomimicry while addressing multi-throughput demands, given the substantial influence of the coculture model on cellular responses triggered by CS. Furthermore, the coculture model exhibited a mutually beneficial protective effect on cells at low CS concentrations within the GCGG unit, yet revealed a mutually amplified damaging effect at higher CS concentrations in contrast to the monoculture model.


Assuntos
Fumar Cigarros , Microfluídica , Técnicas de Cocultura , Células Endoteliais , Biônica , Pulmão , Aerossóis
7.
PLoS One ; 19(3): e0297661, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38442133

RESUMO

Cigarette smoke-induced protein aggregation damages the lung cells in emphysema and COPD; however, lung cancer cells continue to thrive, evolving to persist in the toxic environment. Here, we showed that upon the cigarette smoke condensate exposure, A549 lung cancer cells exhibit better survival and reduced level of protein aggregation when compared to non-cancerous Beas-2B and H-6053 cells. Our data suggests that upregulation of efflux pumps in cancer cells assists in reducing smoke toxicity. Specifically, we demonstrated that inhibition of the ABCG2 transporter in A549 by febuxostat or its downregulation by shRNA-mediated RNA interference resulted in a significant increase in protein aggregation due to smoke exposure.


Assuntos
Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP , Fumar Cigarros , Neoplasias Pulmonares , Agregados Proteicos , Humanos , Células A549 , Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/metabolismo
8.
Int Immunopharmacol ; 131: 111832, 2024 Apr 20.
Artigo em Inglês | MEDLINE | ID: mdl-38460301

RESUMO

Cigarette smoke is widely known as contributing to chronic inflammation underlying several airway diseases, such as chronic obstructive pulmonary disease (COPD) and lung cancer. In our previous studies we found that the lung of both COPD and cancer patients were characterized by the presence and activation of the AIM2 inflammasome. Here, we wanted to investigate the upstream step during the establishment of chronic lung inflammation after cigarette smoke exposure. We took advantage of a mouse model of smoking exposure and public scRNAseq data. We found that AIM2 mRNA was expressed in both alveolar type II, B cells, T regulatory (Treg) and macrophages detected in the lung of non-smokers (n = 4) and smokers (n = 3). The activation of AIM2 in smoking mice by using PolydA:dT did not alter cigarette-smoke-induced alveoli enlargement and mucus production, rather it induced higher recruitment of immunosuppressive cells, such as non-active dendritic cells (DCs), Arginase I+ macrophages, myeloid-derived suppressor cells (MDSC) and Tregs. In addition, the inflammatory environment after AIM2 activation in smoking mice was characterized by higher levels of IL-1α, IL-1ß, IL-33, TNFα, LDH, IL-10 and TGFß. This scenario was not altered after the pharmacological inhibition of both caspase-1 and STING pathway. In conclusion, these data suggest that chronic inflammation after cigarette smoke exposure is associated with AIM2 activation, which could lead towards cigarette smoke-associated lung diseases.


Assuntos
Fumar Cigarros , Doença Pulmonar Obstrutiva Crônica , Humanos , Camundongos , Animais , Inflamassomos/metabolismo , Fumar Cigarros/efeitos adversos , Pulmão/metabolismo , Inflamação , Imunossupressores , Camundongos Endogâmicos C57BL , Proteínas de Ligação a DNA/genética
9.
BMJ Open Respir Res ; 11(1)2024 Mar 09.
Artigo em Inglês | MEDLINE | ID: mdl-38460973

RESUMO

BACKGROUND: While heated tobacco products (HTPs) may affect pulmonary function, the evidence supporting the utility of screening for HTP use in clinical settings is insufficient. We examined the association between HTP use and airway obstruction after switching from cigarettes. METHOD: The study subjects were patients aged ≥20 years undergoing surgery from December 2021 to September 2022 who completed spirometry and reported tobacco (cigarette and HTP) use status during the preoperative assessment. Airway obstruction was defined as forced expiratory volume in 1 s to forced vital capacity ratio below the lower limit of normal. Current tobacco use was defined as past-30-day use. Multivariable Poisson regression analysis was performed to examine the associations between HTP use and airway obstruction by adjusting for demographic characteristics, lifetime cigarette smoking (pack-year) and duration of smoking cessation. RESULTS: Overall (N=2850, 55.4% women, mean age 62.4), 4.6% and 10.7% reported current HTP use and cigarette smoking, respectively. 16.8% had airway obstruction. Airway obstruction was more common among current HTP-only users (adjusted prevalence ratio (APR)=2.32), current cigarette-only smokers (APR=2.57) and current dual users (APR=2.82) than never-tobacco users. Among current tobacco users (N=398), the prevalence of airway obstruction was not significantly different between HTP-only users and cigarette-only smokers. Among former cigarette smokers (>30-day cigarette quitters) (N=1077), current HTP users had 1.42 times the increased prevalence of airway obstruction than never-HTP users after adjusting for cigarette pack-year; a stronger association was observed when the analysis was restricted to ≥5-year cigarette quitters (N=772) (APR=1.96, vs never HTP users). CONCLUSION: Current HTP use was associated with airway obstruction among patients with cancer who had completely switched from cigarettes even after quitting smoking for a long period. Patients should be routinely screened for HTP use and advised to quit any tobacco.


Assuntos
Obstrução das Vias Respiratórias , Fumar Cigarros , Produtos do Tabaco , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Obstrução das Vias Respiratórias/epidemiologia , Obstrução das Vias Respiratórias/etiologia , Fumar Cigarros/epidemiologia , Japão/epidemiologia , Produtos do Tabaco/efeitos adversos
10.
BMC Psychiatry ; 24(1): 201, 2024 Mar 12.
Artigo em Inglês | MEDLINE | ID: mdl-38475757

RESUMO

BACKGROUND: Menthol cigarette use remains a large public health problem and disproportionately affects Black adults in the United States. The Food and Drug Administration has proposed prohibiting menthol flavor in cigarettes to protect public health. However, e-cigarettes are available in menthol flavor and are a popular alternative product adults might switch to if menthol is prohibited in cigarettes. Research is needed to understand how availability of menthol (vs. tobacco) flavored e-cigarettes could impact cigarette use among adults who smoke menthol cigarettes. METHODS: We will recruit 150 adults who currently smoke menthol cigarettes and will randomize them to 1 of 3 conditions modeling different regulatory scenarios. We will recruit equal numbers of participants identifying as Black vs. non-Black and will stratify randomization by race. To promote standardization and adherence, cigarette and e-cigarette products will be provided for 8 weeks based on the assigned condition: (A) no menthol restriction (menthol cigarette and menthol flavored e-cigarette), (B) menthol prohibited in cigarettes only (non-menthol cigarette and menthol flavored e-cigarette), (C) menthol prohibited in both cigarettes and e-cigarettes (non-menthol cigarette and tobacco flavored e-cigarette). A follow-up visit will occur at week 12 to assess tobacco use status. The study aims are to (1) examine the impact of prohibiting menthol flavor in cigarettes and e-cigarettes on smoking behavior and (2) investigate whether outcomes differ by race to understand the impact of menthol policies on Black (vs. non-Black) individuals given high rates of menthol cigarette use in this population. The primary outcome will evaluate changes in the number of cigarettes smoked per day during the 8-week study period and will examine differences by regulatory scenario. Secondary outcomes will compare percent days smoke-free, changes in nicotine dependence, and motivation, confidence, and intentions to quit smoking by the regulatory scenarios. We will examine whether changes in the outcomes differ by Black vs. non-Black participants to compare the magnitude of the effect of the various menthol policy scenarios by race. DISCUSSION: Results will contribute critical information regarding menthol in cigarettes and e-cigarettes to inform regulatory policies that maximize reductions in cigarette smoking and reduce tobacco-related health disparities. TRIAL REGISTRATION: NCT05259566. Yale IRB protocol #2000032211, last approved 12/8/2023.


Assuntos
Fumar Cigarros , Sistemas Eletrônicos de Liberação de Nicotina , Produtos do Tabaco , Adulto , Humanos , Estados Unidos , Mentol , Fumar Cigarros/epidemiologia , Aromatizantes , Controle do Tabagismo , Ensaios Clínicos Controlados Aleatórios como Assunto
11.
Artigo em Inglês | MEDLINE | ID: mdl-38544929

RESUMO

Background: The incidence of chronic obstructive pulmonary disease (COPD) is increasing year by year. Kruppel-like factor 6 (KLF6) plays an important role in inflammatory diseases. However, the regulatory role of KLF6 in COPD has not been reported so far. Methods: The viability of human bronchial epithelial cells BEAS-2B induced by cigarette smoke extract (CSE) was detected by CCK-8 assay. The protein expression of KLF6 and sirtuin 4 (SIRT4) was appraised with Western blot. RT-qPCR and Western blot were applied to examine the transfection efficacy of sh-KLF6 and Oe-KLF6. Cell apoptosis was detected using flow cytometry. The levels of inflammatory factors IL-6, TNF-α and IL-1ß were assessed with ELISA assay. DCFH-DA staining was employed for the detection of ROS activity and the levels of oxidative stress markers SOD, CAT and MDA were estimated with corresponding assay kits. The mitochondrial membrane potential (MMP), adenosine triphosphate (ATP) content and Complex I activity were evaluated with JC-1 staining, ATP colorimetric/fluorometric assay kit and Complex I enzyme activity microplate assay kit. With the application of mitochondrial permeability transition pore detection kit, mPTP opening was measured. Luciferase report assay was employed to evaluate the activity of SIRT4 promoter and chromatin immunoprecipitation (ChIP) to verify the binding ability of KLF6 and SIRT4 promoter. Results: KLF6 expression was significantly elevated in CSE-induced cells. KLF6 was confirmed to suppress SIRT4 transcription. Interference with KLF6 expression significantly inhibited cell viability damage, cell apoptosis, inflammatory response, oxidative stress and mitochondrial dysfunction in CSE-induced BEAS-2B cells, which were all reversed by SIRT4 overexpression. Conclusion: Silencing KLF6 alleviated CSE-induced mitochondrial dysfunction in bronchial epithelial cells by SIRT4 upregulation.


Assuntos
Fumar Cigarros , Doenças Mitocondriais , Doença Pulmonar Obstrutiva Crônica , Sirtuínas , Humanos , Doença Pulmonar Obstrutiva Crônica/metabolismo , Regulação para Cima , Linhagem Celular , Fator 6 Semelhante a Kruppel/genética , Fator 6 Semelhante a Kruppel/metabolismo , Fumar Cigarros/efeitos adversos , Apoptose , Células Epiteliais/metabolismo , Trifosfato de Adenosina/efeitos adversos , Trifosfato de Adenosina/metabolismo , Doenças Mitocondriais/metabolismo , Proteínas Mitocondriais/efeitos adversos , Proteínas Mitocondriais/metabolismo , Sirtuínas/genética
12.
Sci Total Environ ; 923: 171351, 2024 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-38432370

RESUMO

Cigarette smoke contains many chemicals that are harmful to both smokers and non-smokers. Breathing just a little cigarette smoke can be harmful. There are >7000 chemicals in cigarette smoke, at least 250 are known to be harmful and many of them can cause cancer. Currently, many studies reported the types of harmful organic compounds in cigarette smoke; instead, there are almost no works that describe the presence of inorganic compounds. In this work, a cost-effective self-made passive sampler (SMPS) was tested as a tool to collect different types of particulate matter (PM) from cigarette smoke containing metals as hazardous compounds (HCs). To determine the nature of the metals, nonmetals and metalloids as HCs, a direct qualitative analysis of the particulate matter (PM) was conducted without developing any special sample preparation procedure. For that, non-invasive elemental (Scanning Electron Microscope coupled to Energy Dispersive X-ray Spectrometry) and molecular (Raman microscopy) micro-spectroscopic techniques were used. Thanks to this methodology, it was possible to determine in deposited PM, the presence of metals such as Fe, Cr, Ni, Ti, Co, Sn, Zn, Ba, Al, Cu, Zr, Ce, Bi, etc. most of them as oxides but also embedded in different clusters with sulfates, aluminosilicates, even phosphates.


Assuntos
Fumar Cigarros , Metaloides , Humanos , Metaloides/análise , Metais , Material Particulado/análise , Espectrometria por Raios X
13.
BMC Biotechnol ; 24(1): 13, 2024 Mar 08.
Artigo em Inglês | MEDLINE | ID: mdl-38459479

RESUMO

OBJECTIVE: Smoking was a major risk factor for chronic obstructive pulmonary disease (COPD). This study plan to explore the mechanism of Polyphyllin B in lung injury induced by cigarette smoke (CSE) in COPD. METHODS: Network pharmacology and molecular docking were applied to analyze the potential binding targets for Polyphyllin B and COPD. Commercial unfiltered CSE and LPS were used to construct BEAS-2B cell injury in vitro and COPD mouse models in vivo, respectively, which were treated with Polyphyllin B or fecal microbiota transplantation (FMT). CCK8, LDH and calcein-AM were used to detect the cell proliferation, LDH level and labile iron pool. Lung histopathology, Fe3+ deposition and mitochondrial morphology were observed by hematoxylin-eosin, Prussian blue staining and transmission electron microscope, respectively. ELISA was used to measure inflammation and oxidative stress levels in cells and lung tissues. Immunohistochemistry and immunofluorescence were applied to analyze the 4-HNE, LC3 and Ferritin expression. RT-qPCR was used to detect the expression of FcRn, pIgR, STAT3 and NCOA4. Western blot was used to detect the expression of Ferritin, p-STAT3/STAT3, NCOA4, GPX4, TLR2, TLR4 and P65 proteins. 16S rRNA gene sequencing was applied to detect the gut microbiota. RESULTS: Polyphyllin B had a good binding affinity with STAT3 protein, which as a target gene in COPD. Polyphyllin B inhibited CS-induced oxidative stress, inflammation, mitochondrial damage, and ferritinophagy in COPD mice. 16S rRNA sequencing and FMT confirmed that Akkermansia and Escherichia_Shigella might be the potential microbiota for Polyphyllin B and FMT to improve CSE and LPS-induced COPD, which were exhausted by the antibiotics in C + L and C + L + P mice. CSE and LPS induced the decrease of cell viability and the ferritin and LC3 expression, and the increase of NCOA4 and p-STAT3 expression in BEAS-2B cells, which were inhibited by Polyphyllin B. Polyphyllin B promoted ferritin and LC3II/I expression, and inhibited p-STAT3 and NCOA4 expression in CSE + LPS-induced BEAS-2B cells. CONCLUSION: Polyphyllin B improved gut microbiota disorder and inhibited STAT3/NCOA4 pathway to ameliorate lung tissue injury in CSE and LPS-induced mice.


Assuntos
Fumar Cigarros , Microbioma Gastrointestinal , Lesão Pulmonar , Doença Pulmonar Obstrutiva Crônica , Animais , Camundongos , Linhagem Celular , Fumar Cigarros/efeitos adversos , Ferritinas/metabolismo , Inflamação/patologia , Lipopolissacarídeos/efeitos adversos , Pulmão , Lesão Pulmonar/complicações , Lesão Pulmonar/metabolismo , Lesão Pulmonar/patologia , Simulação de Acoplamento Molecular , Doença Pulmonar Obstrutiva Crônica/terapia , Doença Pulmonar Obstrutiva Crônica/tratamento farmacológico , RNA Ribossômico 16S , Fator de Transcrição STAT3/genética , Fator de Transcrição STAT3/metabolismo
14.
Environ Int ; 185: 108521, 2024 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-38508052

RESUMO

Electronic cigarettes (e-cigarettes) have rapidly gained popularity as alternatives to traditional combustible cigarettes. However, their long-term health impact remains uncertain. This study aimed to investigate the effects of chronic exposure to e-cigarette aerosol (ECA) in mice compared to conventional cigarette smoke (CS) exposure. The mice were exposed to air (control), low, medium, or high doses of ECA, or a reference CS dose orally and nasally for eight months. Various cardiovascular and pulmonary assessments have been conducted to determine the biological and prosthetic effects. Histopathological analysis was used to determine structural changes in the heart and lungs. Biological markers associated with fibrosis, inflammation, and oxidative stress were investigated. Cardiac proteomic analysis was applied to reveal the shared and unique protein expression changes in ECA and CS groups, which related to processes such as immune activation, lipid metabolism, and intracellular transport. Overall, chronic exposure to ECA led to adverse cardiovascular and pulmonary effects in mice, although they were less pronounced than those of CS exposure. This study provides evidence that e-cigarettes may be less harmful than combustible cigarettes for the long-term health of the cardiovascular and respiratory systems in mice. However, further human studies are needed to clarify the long-term health risks associated with e-cigarette use.


Assuntos
Fumar Cigarros , Sistemas Eletrônicos de Liberação de Nicotina , Animais , Humanos , Camundongos , Aerossóis/toxicidade , Pulmão , Proteômica
15.
Exp Lung Res ; 50(1): 53-64, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38509754

RESUMO

OBJECTIVE: The aim of this study is to assess the impact of Liver X receptors (LXRs) on airway inflammation, airway remodeling, and lipid deposition induced by cigarette smoke and lipopolysaccharide (LPS) exposure in the lung. METHODS: Wild mice and LXR-deficient mice were exposed to cigarette smoke and LPS to induce airway inflammation and remodeling. In addition, some wild mice received intraperitoneal treatment with the LXR agonist GW3965 before exposure to cigarette smoke and LPS. Lung tissue and bronchoalveolar lavage fluid were collected to evaluate airway inflammation, airway remodeling and lipid deposition. RESULTS: Exposure to cigarette smoke and LPS resulted in airway inflammation, emphysema and lipid accumulation in wild mice. These mice also exhibited downregulated LXRα and ABCA1 in the lung. Treatment with GW3965 mitigated inflammation, remodeling and lipid deposition, while the deletion of LXRs exacerbated these effects. Furthermore, GW3965 treatment following exposure to cigarette smoke and LPS increased LXRα and ABCA1 expression and attenuated MyD88 expression in wild mice. CONCLUSION: LXRs demonstrate the potential to mitigate cigarette smoke and LPS- induced airway inflammation, emphysema and lipid disposition in mice.


Assuntos
Benzoatos , Benzilaminas , Fumar Cigarros , Enfisema , Enfisema Pulmonar , Animais , Camundongos , Remodelação das Vias Aéreas , Líquido da Lavagem Broncoalveolar , Fumar Cigarros/efeitos adversos , Enfisema/metabolismo , Inflamação/tratamento farmacológico , Inflamação/metabolismo , Lipopolissacarídeos/farmacologia , Receptores X do Fígado/metabolismo , Pulmão/metabolismo , Camundongos Endogâmicos C57BL
16.
BMC Public Health ; 24(1): 668, 2024 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-38429672

RESUMO

BACKGROUND: Despite the harmful effects of smoking, there have been few studies to pinpoint the factors of this habit, and little is known about it in the East African region. For this reason, this study sought to determine the frequency and factors of cigarette smoking among men in the region. METHODS: Data from recent demographic and health surveys carried out in ten East African countries between 2015 and 2022 were analyzed in this study. Data from 87,022 men was collected. The key factors affecting the smoking rates in the area were investigated using binary and multiple multinomial logistic regression. To ascertain if variables were statistically significant in the final model for binary regression and multiple regression, P values of ≤ 0.2 and < 0.05 were used respectively. RESULTS: Overall, about 14.69% of people currently smoke cigarettes. Of this about 11.03 (95% CI = 10.82, 11.24) was for daily active tobacco use. As compared to < 26-year-old men, men with an age range of 26-35 years (RRR = 2.17, 95% CI: 2.01,2.34), 36-45 years (RRR = 2.82, 95% CI: 2.60, 3.07), and > 45 years old (RRR = 3.68, 95% CI: 3.38, 4.02), were using cigarettes daily rather than no-smoking cigarettes. Men who had begun their first sexual intercourse at the age of 7-19 years (RRR = 6.27,95% CI, 5.35,7.35), 20-25 years (RRR = 4.01, 95% CI, 3.40,4.72), and greater than 25 years old (RRR = 3.08, 95% CI, 2.55,3.71) have shown a higher relative risk ratio to smoke cigarette daily rather than using not smoke cigarette respectively, married (RRR = 0.86, 95% CI, 0.79,0.93), divorced or widowed (RRR = 2.51, 95% CI, 2.27,2.77), middle wealth index (RRR = 2.11, 95% CI 1.98,2.24), and rich (RRR = 1.44, 95% CI, 1.34,1.54), secondary/higher education (RRR = 0.72, 05% CI, 0.66,0.77), rural men (RRR = 0.69, 95% CI, 0.65,0.73), employed men (RRR = 1.26,95% CI, 1.17,1.36), mass media exposure (RRR = 0.76, 95% CI, 0.73,0.81), men who have one sex partner (RRR = 1.23,95% CI,1.13,1.35), and more than one sex partner (RRR = 1.63, 95% CI, 1.47,1.79) more times as compared to those participants who had no sex partner respectively. CONCLUSIONS: Men in East African nations were substantially more likely to smoke cigarettes if they were older, had less education, had a higher wealth index, were divorced or widowed, had many sexual relationships, had early sexual activity, resided in an urban area, were employed, or had no media exposure. The identified factors should be considered by policymakers and public health professionals to lower smoking initiation and increase smoking cessation among men.


Assuntos
Fumar Cigarros , Produtos do Tabaco , Masculino , Humanos , Adulto , Criança , Adolescente , Adulto Jovem , Pessoa de Meia-Idade , Fumar Cigarros/epidemiologia , Prevalência , Fumar/epidemiologia , África Oriental/epidemiologia
17.
BMJ Open ; 14(2): e070749, 2024 Feb 26.
Artigo em Inglês | MEDLINE | ID: mdl-38413149

RESUMO

OBJECTIVES: To describe the prevalence of school-based tobacco prevention programme exposure among adolescents in low-income and middle-income countries (LMICs) and its association with psychosocial predictors of smoking. DESIGN: Analysis of pooled cross-sectional data. SETTING: Global Youth Tobacco Survey (GYTS), conducted in 38 LMICs. PARTICIPANTS: This was a pooled analysis of data involving a total of 132 755 adolescent respondents to GYTS in 38 LMICs across Africa, Europe and Central/South America between 2014 and 2017. EXPOSURE AND OUTCOME MEASURES: The primary independent variable for this study was self-reported exposure to school-based tobacco prevention programmes in the past year. Five psychosocial determinants of smoking were explored as outcomes: perceived addictiveness of nicotine, perceived harm of secondhand smoke exposure, support for restricting cigarette smoking at public indoor locations, support for restricting cigarette smoking at public outdoor areas and self-reported prediction of enjoying cigarette smoking. Multivariable logistic regression models were used to examine the relationship between exposure to school-based tobacco prevention programmes and study outcomes, controlling for sociodemographic and smoking-related characteristics of respondents. RESULTS: Overall, 59.1% of adolescents in LMICs self-reported exposure to school-based tobacco prevention programmes. The country-specific prevalence of adolescent exposure to school-based tobacco interventions ranged from 24.9% in the Comoros to 99.3% in Turkmenistan. Exposure to school-based tobacco interventions was significantly associated with greater secondhand smoke harm perceptions (adjusted OR (AOR): 1.69; 95% CI: 1.69 to 1.70), perceptions of addictiveness (AOR: 1.37; 95% CI: 1.36 to 1.37) and supporting tobacco use restrictions indoors (AOR: 1.70; 95% CI: 1.69 to 1.70) and outdoors (AOR: 1.59; 95% CI: 1.59 to 1.60). Exposure to school-based tobacco interventions was associated with lower odds of anticipating enjoying cigarette smoking (AOR: 0.76; 95% CI: 0.76 to 0.76). CONCLUSION: Exposure to tobacco prevention programmes in schools is suboptimal in LMICs. Given the protective associations described in this study from school-based tobacco prevention programme exposure, it is imperative that national governments implement school-based programmes into ongoing tobacco control measures.


Assuntos
Fumar Cigarros , Poluição por Fumaça de Tabaco , Humanos , Adolescente , Estudos Transversais , Países em Desenvolvimento , Poluição por Fumaça de Tabaco/prevenção & controle , Inquéritos e Questionários , Fumar Cigarros/epidemiologia , Produtos do Tabaco
19.
Nutrients ; 16(3)2024 Jan 31.
Artigo em Inglês | MEDLINE | ID: mdl-38337717

RESUMO

Lung inflammation and alveolar enlargement are the major pathological conditions of chronic obstructive pulmonary disease (COPD) patients. Rice bran oil (RBO), a natural anti-inflammatory and antioxidative agent, has been used for therapeutic purposes in several inflammatory diseases. This study aimed to investigate the anti-inflammatory and antioxidative effect of RBO on a cigarette smoke extract (CSE)-induced emphysema model in mice. The results indicated that CSE significantly induced airspace enlargement in mouse lung. Increased inflammatory cells, macrophage, and TNF-alpha levels in bronchoalveolar lavage fluid (BALF) were noticed in CSE-treated mice. RBO (low and high dose)-supplemented mice showed decreased total BALF inflammatory cell, macrophage, and neutrophil numbers and TNF-alpha levels (p < 0.05). Additionally, the administration of RBO decreased the mean linear alveolar intercept (MLI) in the CSE-treated group. Additionally, RBO treatment significantly increased the total antioxidant capacity in both mouse BALF and serum. However, RBO did not have an effect on the malondialdehyde (MDA) level. These findings suggested that RBO treatment ameliorates lung inflammation in a CSE-induced emphysema mice model through anti-inflammatory and antioxidant pathways. Therefore, the supplementation of RBO could be a new potential therapeutic to relieve the severity of COPD.


Assuntos
Fumar Cigarros , Enfisema , Pneumonia , Doença Pulmonar Obstrutiva Crônica , Enfisema Pulmonar , Humanos , Camundongos , Animais , Antioxidantes/metabolismo , Pulmão/patologia , Óleo de Farelo de Arroz/farmacologia , Fator de Necrose Tumoral alfa/metabolismo , Fumar Cigarros/efeitos adversos , Enfisema Pulmonar/induzido quimicamente , Enfisema Pulmonar/tratamento farmacológico , Doença Pulmonar Obstrutiva Crônica/metabolismo , Anti-Inflamatórios/uso terapêutico , Pneumonia/tratamento farmacológico , Líquido da Lavagem Broncoalveolar , Enfisema/induzido quimicamente , Enfisema/tratamento farmacológico , Produtos do Tabaco
20.
Artigo em Inglês | MEDLINE | ID: mdl-38397715

RESUMO

INTRODUCTION: Smoking-related diseases affect 16 million Americans, causing approximately 480,000 deaths annually. The prevalence of cigarette smoking varies regionally across the United States, and previous research indicates that regional rates of smoking-related diseases demonstrate a negative association with altitude. The purpose of this study was to determine the relationship between altitude and the prevalence of cigarette smoking by county (N = 3106) in the United States. We hypothesized that smoking prevalence among adults would be negatively associated with mean county altitude. METHODS: A multivariate linear regression was performed to examine the relationship between county-level mean altitude and county smoking rate. Covariates were individually correlated with 2020 smoking data, and significant associations were included in the final model. RESULTS: The multivariate linear regression indicated that the county-level smoking rates are significantly reduced at high altitudes (p < 0.001). The model accounted for 89.5% of the variance in smoking prevalence, and for each 1000-foot increase in altitude above sea level, smoking rates decreased by 0.143%. Based on multivariate linear regression, the following variables remained independently and significantly associated: race, sex, educational attainment, socioeconomic status, unemployment, physical inactivity, drinking behavior, mental distress, and tobacco taxation. CONCLUSIONS: Our results indicate that smoking rates are negatively associated with altitude, which may suggest that altitude affects the pharmacokinetics, pharmacodynamics, and mechanistic pathways involved in cigarette use. Further research is needed to explore the relationship between altitude and smoking and how altitude may serve as a protective factor in the acquisition and maintenance of tobacco use disorders.


Assuntos
Altitude , Fumar Cigarros , Adulto , Humanos , Estados Unidos/epidemiologia , Classe Social , Escolaridade , Fumar Cigarros/epidemiologia , Comportamento Sedentário , Prevalência
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