scholarly journals Is the cellular response to cigarette smoke predictive of the phenotypic variation of COPD?

2011 ◽  
Vol 300 (6) ◽  
pp. L809-L810 ◽  
Author(s):  
Gye Young Park ◽  
John W. Christman
Keyword(s):  
Cigarette Smoking ◽  
Phenotypic Variation ◽  
Cellular Response ◽  
Vascular Diseases ◽  
Cell Types ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Immune Effector ◽  
Effector Cells ◽  
Organ Systems

the adverse health consequences of cigarette smoking are not limited to the lung but also include effects on multiple other organ systems that are exposed directly or indirectly to the hazardous gaseous and soluble compounds generated by burning tobacco. Cigarette smoking (CS) is a risk factor for many major diseases including chronic obstructive pulmonary disease (COPD), atherosclerosis, cerebral and coronary vascular diseases, hypertension, and many types of cancer. Within the diagnosis category of COPD, it is widely recognized that there is substantial phenotypic heterogeneity with respect to both pulmonary and extrapulmonary manifestations. To understand the variability in responses to CS, it becomes essential to decipher the involved mechanisms at a cellular and molecular level that contribute to cigarette-related pathology. In this issue of the Journal, there are three papers ( 1 , 4 , 6 ) that provide insight regarding the molecular pathogenesis of CS-related COPD that could be related to phenotypic variation, by examining three classes of cell types of lung: endothelial cells, epithelial cells, and immune effector cells.

scholarly journals Signaling Control of Mucociliary Epithelia: Stem Cells, Cell Fates, and the Plasticity of Cell Identity in Development and Disease

2021 ◽  
pp. 1-18
Author(s):  
Peter Walentek
Keyword(s):  
Stem Cells ◽  
Mucociliary Clearance ◽  
Cell Types ◽  
Secretory Cells ◽  
Chronic Obstructive ◽  
Cell Identity ◽  
Obstructive Pulmonary Disease ◽  
Congenital Diseases ◽  
Inhaled Particles ◽  
Mucociliary Epithelia

Mucociliary epithelia are composed of multiciliated, secretory, and stem cells and line various organs in vertebrates such as the respiratory tract. By means of mucociliary clearance, those epithelia provide a first line of defense against inhaled particles and pathogens. Mucociliary clearance relies on the correct composition of cell types, that is, the proper balance of ciliated and secretory cells. A failure to generate and to maintain correct cell type composition and function results in impaired clearance and high risk to infections, such as in congenital diseases (e.g., ciliopathies) as well as in acquired diseases, including asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF). While it remains incompletely resolved how precisely cell types are specified and maintained in development and disease, many studies have revealed important mechanisms regarding the signaling control in mucociliary cell types in various species. Those studies not only provided insights into the signaling contribution to organ development and regeneration but also highlighted the remarkable plasticity of cell identity encountered in mucociliary maintenance, including frequent trans-differentiation events during homeostasis and specifically in disease. This review will summarize major findings and provide perspectives regarding the future of mucociliary research and the treatment of chronic airway diseases associated with tissue remodeling.

scholarly journals Exposure to the gut microbiota from cigarette smoke-exposed mice exacerbates cigarette smoke extract-induced inflammation in zebrafish larvae

2021 ◽  
Author(s):  
Simone Morris ◽  
Kathryn Wright ◽  
Vamshikrishna Malyla ◽  
Warwick J Britton ◽  
Philip M Hansbro ◽  
...  
Keyword(s):  
Cigarette Smoking ◽  
Gut Microbiota ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Zebrafish Larvae ◽  
Modifying Factors ◽  
Physiological Processes ◽  
Inflammatory Phenotype

AbstractCigarette smoke (CS)-induced inflammation leads to a range of diseases including chronic obstructive pulmonary disease and cancer. Environmental factors including gut microbiota make up are major modifying factors that determine the severity of cigarette smoke-induced pathology. Adult zebrafish display increased inflammatory cytokine transcription when exposed to cigarette smoke extract (CSE) but incongruously do not produce a mucosal leukocytic inflammation phenotype. Zebrafish embryos and larvae have been used to model the effects of cigarette smoking on a range of physiological processes and offer an amenable platform for screening modifiers of cigarette smoke-induced pathologies. Here we exposed zebrafish larvae to CSE and showed that it was toxic and we characterised a CSE-induced leukocytic inflammatory phenotype with increased neutrophilic and macrophage responses. The CSE-induced phenotype was exacerbated by co-exposure to microbiota from the faeces of CS-exposed mice, but not control mice. Microbiota could be recovered from the gut of zebrafish and studied in isolation. This demonstrates the utility of the zebrafish-CSE exposure platform for identifying environmental modifiers of cigarette smoking-associated pathology and demonstrates that the CS-exposed mouse gut microbiota potentiates the inflammatory effects of CSE across host species.

The rise of electronic nicotine delivery systems and the emergence of electronic-cigarette-driven disease

2020 ◽  
Vol 319 (4) ◽  
pp. L585-L595 ◽  
Author(s):  
Kielan Darcy McAlinden ◽  
Mathew Suji Eapen ◽  
Wenying Lu ◽  
Pawan Sharma ◽  
Sukhwinder Singh Sohal
Keyword(s):  
United States ◽  
Cigarette Smoking ◽  
Electronic Cigarettes ◽  
Scientific Evidence ◽  
The United States ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Cellular Processes ◽  
Increased Risk

In 2019, the United States experienced the emergence of the vaping-associated lung injury (VALI) epidemic. Vaping is now known to result in the development and progression of severe lung disease in the young and healthy. Lack of regulation on electronic cigarettes in the United States has resulted in over 2,000 patients and 68 deaths. We examine the clinical representation of VALI and the delve into the scientific evidence of how deadly exposure to electronic cigarettes can be. E-cigarette vapor is shown to affect numerous cellular processes, cellular metabolism, and cause DNA damage (which has implications for cancer). E-cigarette use is associated with a higher risk of developing crippling lung conditions such as chronic obstructive pulmonary disease (COPD), which would develop several years from now, increasing the already existent smoking-related burden. The role of vaping and virus susceptibility is yet to be determined; however, vaping can increase the virulence and inflammatory potential of several lung pathogens and is also linked to an increased risk of pneumonia. As it has emerged for cigarette smoking, great caution should also be given to vaping in relation to SARS-CoV-2 infection and the COVID-19 pandemic. Sadly, e-cigarettes are continually promoted and perceived as a safer alternative to cigarette smoking. E-cigarettes and their modifiable nature are harmful, as the lungs are not designed for the chronic inhalation of e-cigarette vapor. It is of interest that e-cigarettes have been shown to be of no help with smoking cessation. A true danger lies in vaping, which, if ignored, will lead to disastrous future costs.

Chronic Obstructive Pulmonary Disease Is Common in Never-smoking Patients with Primary Sjögren Syndrome

2015 ◽  
Vol 42 (3) ◽  
pp. 464-471 ◽  
Author(s):  
Anna Matilda Nilsson ◽  
Sandra Diaz ◽  
Elke Theander ◽  
Roger Hesselstrand ◽  
Eeva Piitulainen ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Cigarette Smoking ◽  
Disease Activity ◽  
Lung Disease ◽  
Respiratory Symptoms ◽  
Sjögren Syndrome ◽  
Chronic Obstructive ◽  
Sjogren Syndrome ◽  
Obstructive Pulmonary Disease ◽  
Primary Sjögren Syndrome

Objective.To assess the prevalence of chronic obstructive pulmonary disease (COPD) in patients with primary Sjögren syndrome (pSS) and to study the association of COPD with cigarette smoking, radiographic features, respiratory symptoms, disease activity, and laboratory inflammatory and serological features in patients with pSS.Methods.Fifty-one consecutive patients with pSS (mean age 60 yrs, range 29–82 yrs, 49 women) were assessed by pulmonary function tests (PFT). The PFT results were compared with previously studied population-based controls, standardizing results with regard to sex, age, height, weight, and cigarette smoking. In addition, patients with pSS were assessed by computed tomography of the chest, the European League Against Rheumatism Sjögren Syndrome Disease Activity Index and Patient Reported Index, the St. George’s Respiratory Questionnaire (which evaluates respiratory symptoms), and by laboratory inflammatory and serological tests.Results.Forty-one percent of all patients with pSS and 30% of the never-smoking patients with pSS fulfilled the Global Initiative for Chronic Obstructive Lung Disease criteria for COPD. Vital capacity (VC), forced expiratory volume in 1 s (FEV1), FEV1/VC ratio, and DLCO were significantly decreased while residual volume (RV) and the RV/total lung capacity ratio were significantly increased in patients with pSS. Moderate correlations between PFT results, symptoms, and disease activity were found. However, laboratory inflammatory and serological features were poorly associated with PFT results in patients with pSS.Conclusion.COPD was a common finding in patients with pSS, even among never-smoking patients. An obstructive pattern was the predominant PFT finding in patients with pSS, although a superimposed restrictive lung disease could not be excluded. The results suggest that the disease per se is involved in the development of COPD in pSS.

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