scholarly journals Smoking and COPD: Endothelium-Related and Neuro-mediated Emphysema Mechanisms

Author(s):  
Vera Nevzorova ◽  
Tatiana Brodskaya ◽  
Eugeny Gilifanov

This chapter describes endothelium-related and neuro-mediated mechanisms of emphysema development in chronic obstructive pulmonary disease (COPD) and smoking on the basis of previously completed studies, literature data, and own researches. As components of neurogenic inflammation in the processes of tissue remodeling in emphysema, we describe the distribution and activity of the substance P, neurokinin-1 and its receptor, tissue metalloproteinases and their tissue inhibitors in the lungs during the entire experimental period, the modeling of COPD in rats with a smoking model. We also analyzed the content of neurokinin system markers, the localization, and markers of tissue metalloproteinases in human lung tissue structures. We have confidence that there is a special morphofunctional continuum of development of lower respiratory tract remodeling in response to chronic exposure to tobacco smoke and the development of inflammation in COPD. New data suggest that imbalance of neuro-mediated interactions, alteration of vasomotoric signaling mechanisms, secretion, mucociliary clearance, cytoprotection involving substance P-dependent components with impaired content, and development of dystopia of matrix metalloproteinases and their tissue inhibitors are involved in the initiation of morphological restructuring. Research in this direction should be continued to allow approaches to the development of preventive and therapeutic strategies for emphysema.

1996 ◽  
Vol 81 (4) ◽  
pp. 1715-1722 ◽  
Author(s):  
A. C. Bonham ◽  
K. S. Kott ◽  
J. P. Joad

Bonham, A. C., K. S. Kott, and J. P. Joad. Sidestream smoke exposure enhances rapidly adapting receptor responses to substance P in young guinea pigs. J. Appl. Physiol. 81(4): 1715–1722, 1996.—We determined the effect of sidestream tobacco smoke (SS) exposure on responses of lung rapidly adapting receptors (RARs), peak tracheal pressure (Ptr), and arterial blood pressure (ABP) to substance P in young guinea pigs. Guinea pigs were exposed to SS or filtered air from day 8 to days 41–45 of life. They were then anesthetized and given three doses of intravenous substance P (1.56–4.94 nmol/kg). SS exposure augmented substance P-evoked increases in RAR activity ( P = 0.029 by analysis of variance) but not substance P-evoked increases in peak Ptr or decreases in ABP. Neurokinin 1-receptor blockade (CP-96345, 400 nmol/kg) attenuated substance P-evoked increases in RAR activity ( P = 0.001) and ABP ( P = 0.009) but not in peak Ptr ( P = 0.06). Thus chronic exposure to SS in young guinea pigs exaggerates RAR responsiveness to substance P. The findings may help explain the increased incidence of airway hyperresponsiveness and cough in children chronically exposed to environmental tobacco smoke.


2021 ◽  
Vol 8 (1) ◽  
pp. e000761
Author(s):  
Hendrik Johannes Prins ◽  
Ruud Duijkers ◽  
Johannes M A Daniels ◽  
Thys van der Molen ◽  
Tjip S van der Werf ◽  
...  

BackgroundWe developed the chronic obstructive pulmonary disease (COPD)-Lower Respiratory Tract Infection-Visual Analogue Score (c-LRTI-VAS) in order to easily quantify symptoms during exacerbations in patients with COPD. This study aimed to validate this score.MethodsIn our study, patients with stable COPD as well as those with an acute exacerbations of COPD (AECOPD) were included. The results of c-LRTI-VAS were compared with other markers of disease activity (lung function parameters, oxygen saturation and two health related quality of life questionnaires (St Georges Respiratory Questionnaire (SGRQ) and Clinical COPD Questionnaire (CCQ)) and validity, reliability and responsiveness were assessed.ResultsEighty-eight patients with clinically stable COPD and 102 patients who had an AECOPD completed the c-LRTI-VAS questionnaire. When testing on two separate occasions for repeatability, no statistically significant difference between total scores was found 0.143 (SD 5.42) (p=0.826). Internal consistency was high across items (Cronbach’s apha 0.755). Correlation with SGRQ and CCQ total scores was moderate to high. After treatment for hospitalised AECOPD, the mean c-LRTI-VAS total score improved 8.14 points (SD 9.13; p≤0.001).Conclusionsc-LRTI-VAS showed proper validity, responsiveness to change and moderate to high correlation with other questionnaires. It, therefore, appears a reliable tool for symptom measurement during AECOPD.Trial registration numberNCT01232140.


2019 ◽  
Vol 9 (24) ◽  
Author(s):  
Lalita Fernandes ◽  
Shraddha Rane ◽  
Suresh Mandrekar ◽  
Anthony Menezes Mesquita

Background. Chronic obstructive pulmonary disease (COPD) is an inflammatory disease with predominant involvement of neutrophils, macrophages and CD8+ lymphocytes. Eosinophilic airway inflammations are reported in stable state and during acute exacerbations of tobacco smoke-associated COPD (TS-COPD). Women exposed to biomass fuel smoke are known to have eosinophils in sputum. However, little is known about the sputum cellular inflammatory profile in biomass fuel smoke-associated COPD (BMS-COPD). We therefore aimed to compare the sputum cellular inflammatory profile in tobacco smoke- and biomass smoke-associated COPD. Methods. The study was conducted in a tertiary care hospital in Goa, India. A total of 113 patients with stable COPD reporting to the outpatient pulmonary clinic were recruited. All participants were ≥ 40 years of age. Sputum induction studies were performed by the method of Pizzichini et al. after baseline subject characterization. Significant eosinophilia was defined as induced sputum eosinophils ≥ 3%. Results. There were 85 TS-COPD and 28 BMS-COPD patients. The mean age [standard deviation (SD)] was 64.7 (7.8) and 63.0 years (8.3), p = 0.32 in TS and BMS-COPD, respectively. Eighteen subjects (21.1%) were female smokers. The smoking pack-year median [interquartile range (IQR)] was 36 (20, 58) and hour-years of biomass smoke exposure mean (SD) was 192.4 (61). The TS-COPD and BMS-COPD cases showed a post-bronchodilator forced expiratory volume in one second (FEV1%) mean (SD) of 57.9 (17.1), and 62.6 (19.4), p= 0.22, respectively. Both groups had similar symptoms and severity of disease. Induced sputum total cell count per gram of sputum × 106 mean (SD) was 3.05 (1.53) for TS-COPD, and 2.55(1.37) for BMS-COPD p=0.12. The neutrophils % mean (SD) was 86.4 (16.5) and 87.9 (10.2), p = 0.64; eosinophils % median (IQR) was 2.5 (1, 10) and 8 (2, 12.8), p = 0.07; lymphocytes % median (IQR) was 0 (0, 0.75) and 0 (0, 1) p = 0.13; macrophages % median (IQR) was 2.5 (0.75, 5.7) and 1 (0, 4.7) p = 0.13; and significant eosinophilia (eosinophils ≥3%) was 42 (49.4%) and 20 (71%), p=0.04, for TS-COPD and BMS-COPD, respectively. Conclusions. For similar severity of disease and clinical symptoms, significant eosinophilic inflammation was observed in stable BMS-COPD, while both groups had similar neutrophilic inflammation. Participant Consent. Obtained. Ethics Approval. The study was approved by the Institutional Ethics Committee of the Goa Medical College, Goa, India. Competing Interests. The authors declare no competing financial interests.


2020 ◽  
Author(s):  
Qiuyu Li ◽  
Yizhang Zhu ◽  
Aiyuan Zhou ◽  
Yuxin Yin

Abstract Identification of the dysfunctional genes in human lung from patients with Chronic obstructive pulmonary disease (COPD) will help up to understand the pathology of this disease. Here, using transcriptomic data of lung tissue for 91 COPD cases and 182 matched healthy controls from the Genotype-Tissue Expression (GTEx) database. Employing a stringent model controlling for known covariates and hidden confounders, we identified 1,359 significant differentially expressed genes (DEG) with 707 upregulated and 602 downregulated respectively. We evaluated the identified DEGs in an independent microarray cohort of 219 COPD and 108 controls, demonstrating the robustness of our result. Functional annotation of COPD-associated genes highlighted the activation of complement cascade, dysregulation of inflammatory response and extracellular matrix organization in the COPD patients. In addition, we identified several novel key-hub genes involved in the COPD pathogenesis using a network analysis method. In summary, our study represents the comprehensive analysis of gene expression on COPD with the largest sample size providing great resource for the molecular research in the COPD community.


Author(s):  
Kostas Giokas ◽  
Dimitra Iliopoulou ◽  
Ioannis Makris ◽  
Dimitris Koutsouris

Chronic Obstructive Pulmonary Disease (COPD) is a progressive pulmonary disease characterized by reduction in airflow and is not fully reversible. COPD is the major cause of mortality and increased levels of disability, particularly in the elderly. Symptoms vary among individuals and include breathlessness, dyspnea, abnormal sputum and chronic cough. Exposure to tobacco smoke is by far the most important risk factor in the development of COPD and is associated with high levels of morbidity and mortality. In this chapter the authors will present a system for the integrated care of COPD focusing on prevention and intervention.


2020 ◽  
Vol 7 (7) ◽  
Author(s):  
Eric J Chow ◽  
Melissa A Rolfes ◽  
Ruth L Carrico ◽  
Stephen Furmanek ◽  
Julio A Ramirez ◽  
...  

Abstract Background Preventing severe complications of influenza such as hospitalization is a public health priority; however, estimates of influenza vaccine effectiveness (VE) against influenza-associated acute lower respiratory tract infection (LRTI) hospitalizations are limited. We examined influenza VE against influenza-associated LRTIs in hospitalized adult patients. Methods We retrospectively analyzed data from a randomized trial of oseltamivir treatment in adults hospitalized with LRTI in Louisville, Kentucky, from 2010 to 2013. Patients were systematically tested for influenza at the time of enrollment. We estimated VE as 1 – the adjusted odds ratio (aOR) of antecedent vaccination in influenza-positives vs negatives × 100%. Vaccination status was obtained by patient self-report. Using logistic regression adjusting for age, sex, season, timing of illness, history of chronic lung disease, and activities of daily living, we estimated VE against hospitalized influenza-associated LRTIs and community-acquired pneumonia (CAP) with radiographic findings of infiltrate. Results Of 810 patients with LRTI (median age, 62 years), 184 (23%) were influenza-positive and 57% had radiographically confirmed CAP. Among influenza-positives and -negatives, respectively, 61% and 69% were vaccinated. Overall, 29% were hospitalized in the prior 90 days and >80% had comorbidities. Influenza-negatives were more likely to have a history of chronic obstructive pulmonary disease than influenza-positives (59% vs 48%; P = .01), but baseline medical conditions were otherwise similar. Overall, VE was 35% (95% CI, 4% to 56%) against influenza-associated LRTI and 51% (95% CI, 13% to 72%) against influenza-associated radiographically confirmed CAP. Conclusions Vaccination reduced the risk of hospitalization for influenza-associated LRTI and radiographically confirmed CAP. Clinicians should maintain high rates of influenza vaccination to prevent severe influenza-associated complications.


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