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Pathogenesis of COPD

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https://www.readbyqxmd.com/read/28615935/serum-inflammatory-biomarkers-and-clinical-outcomes-of-copd-exacerbation-caused-by-different-pathogens
#1
Theerasuk Kawamatawong, Apitch Apiwattanaporn, Warisara Siricharoonwong
BACKGROUND AND OBJECTIVE: COPD exacerbation is characterized by worsening of symptoms, warranting change in treatment. Systemic and airway inflammation play roles in the pathogenesis of COPD exacerbation. We hypothesized whether increased serum inflammatory biomarkers are associated with the clinical outcomes of COPD exacerbation caused by different infectious pathogens. METHODS: COPD patients with exacerbation were recruited from a hospital emergency department during 2014-2015...
2017: International Journal of Chronic Obstructive Pulmonary Disease
https://www.readbyqxmd.com/read/28599297/long-term-cigarette-smoke-exposure-inhibits-histone-deacetylase-2-expression-and-enhances-the-nuclear-factor-%C3%AE%C2%BAb-activation-in-skeletal-muscle-of-mice
#2
Dongmei Huang, Zhiying Ma, Yili He, Ying Xiao, Honglin Luo, Qiuli Liang, Xiaoning Zhong, Jing Bai, Zhiyi He
Long-term cigarette smoke induces lung inflammatory injury and chronic obstructive pulmonary disease (COPD), associated with skeletal muscle inflammation. This study aimed at investigating how cigarette smoke promotes skeletal muscle inflammation and its molecular pathogenesis. Mice were exposed to air or cigarette smoke for 12 or 24 weeks, and C2C12 cells were stimulated with cigarette smoke extract (CSE). The mass and function, myotube formation, inflammatory cytokine production, histone deacetylase 2 (HDAC2) and nuclear factor-κB (NF-κB) p65 expression were detected in the gastrocnemius muscles of mice and C2C12 cells...
May 23, 2017: Oncotarget
https://www.readbyqxmd.com/read/28596293/the-uncoupling-of-autophagy-and-zinc-homeostasis-in-airway-epithelial-cells-as-a-fundamental-contributor-to-copd
#3
Eugene Roscioli, Hai Bac Tran, Hubertus Jersmann, Phan Tien Nguyen, Emily Hopkins, Susan Elizabeth Lester, Nigel Farrow, Peter D Zalewski, Paul N Reynolds, Sandra Hodge
The proper regulation of Zinc (Zn) trafficking proteins and the cellular distribution of Zn is critical for the maintenance of autophagic processes. However, there have been no studies which have examined Zn dyshomeostasis and the disease-related modulation of autophagy observed in the airways afflicted with COPD. We hypothesized that dysregulated autophagy in airway epithelial cells (AEC) is related to Zn dysregulation in cigarette smoke (CS)-induced COPD. We applied a human ex vivo air-liquid interface model, a murine model of smoke-exposure, and human lung tissues, and investigated Zn, ZIP1 and ZIP2 Zn-influx proteins, autophagy (Microtubule-associated 1A/1B-light chain-3 (LC3), Beclin-1), autophagic flux (Sequestosome), apoptosis (Bcl2; X-Linked Inhibitor of Apoptosis (XIAP), Poly (ADP)-ribose Polymerase (PARP)), and inflammation (TSLP, RANTES, and IL-1β)...
June 8, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28589151/advanced-role-of-neutrophils-in-common-respiratory-diseases
#4
REVIEW
Jinping Liu, Zhiqiang Pang, Guoqiang Wang, Xuewa Guan, Keyong Fang, Ziyan Wang, Fang Wang
Respiratory diseases, always being a threat towards the health of people all over the world, are most tightly associated with immune system. Neutrophils serve as an important component of immune defense barrier linking innate and adaptive immunity. They participate in the clearance of exogenous pathogens and endogenous cell debris and play an essential role in the pathogenesis of many respiratory diseases. However, the pathological mechanism of neutrophils remains complex and obscure. The traditional roles of neutrophils in severe asthma, chronic obstructive pulmonary diseases (COPD), pneumonia, lung cancer, pulmonary fibrosis, bronchitis, and bronchiolitis had already been reviewed...
2017: Journal of Immunology Research
https://www.readbyqxmd.com/read/28588349/distinct-roles-of-wnt-%C3%AE-catenin-signaling-in-the-pathogenesis-of-chronic-obstructive-pulmonary-disease-and-idiopathic-pulmonary-fibrosis
#5
REVIEW
Juan Shi, Feng Li, Meihui Luo, Jun Wei, Xiaoming Liu
Wnt signaling pathways are tightly controlled under a physiological condition, under which they play key roles in many biological functions, including cell fate specification and tissue regeneration. Increasing lines of evidence recently demonstrated that a dysregulated activation of Wnt signaling, particularly the Wnt/β-catenin signaling, was involved in the pathogenesis of chronic pulmonary diseases, such as chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF). In this respect, Wnt signaling interacts with other cellular signaling pathways to regulate the initiation and pathogenic procedures of airway inflammation and remodeling, pulmonary myofibroblast proliferation, epithelial-to-mesenchymal transition (EMT), and development of emphysema...
2017: Mediators of Inflammation
https://www.readbyqxmd.com/read/28588027/exogenous-neutrophil-elastase-enters-bronchial-epithelial-cells-and-suppresses-cigarette-smoke-extract-induced-heme-oxygenase-1-by-cleaving-sirtuin-1
#6
Kyoung-Hee Lee, Jiyeong Jeong, Yoon-Jung Koo, An-Hee Jang, Chang-Hoon Lee, Chul-Gyu Yoo
An imbalance between oxidative stress and antioxidant activity plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cigarette smoke, a major risk factor of COPD, induces cellular oxidative stress, but levels of antioxidants such as heme oxygenase-1 (HO-1) are reduced in individuals with severe COPD. In this study, we evaluated the molecular mechanism of reduced HO-1 expression in human bronchial epithelial cells. We found that cigarette smoke extract (CSE) increases HO-1 levels via activation of NFE2-related factor 2 (Nrf2)...
June 6, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28575117/gene-and-metabolite-time-course-response-to-cigarette-smoking-in-mouse-lung-and-plasma
#7
Mikaela A Miller, Thomas Danhorn, Charmion I Cruickshank-Quinn, Sonia M Leach, Sean Jacobson, Matthew J Strand, Nichole A Reisdorph, Russell P Bowler, Irina Petrache, Katerina Kechris
Prolonged cigarette smoking (CS) causes chronic obstructive pulmonary disease (COPD), a prevalent serious condition that may persist or progress after smoking cessation. To provide insight into how CS triggers COPD, we investigated temporal patterns of lung transcriptome expression and systemic metabolome changes induced by chronic CS exposure and smoking cessation. Whole lung RNA-seq data was analyzed at transcript and exon levels from C57Bl/6 mice exposed to CS for 1- or 7 days, for 3-, 6-, or 9 months, or for 6 months followed by 3 months of cessation using age-matched littermate controls...
2017: PloS One
https://www.readbyqxmd.com/read/28559466/inhaled-drug-therapy-2016-the-year-in-review
#8
Rajiv Dhand
Some recent salient publications related to inhaled drug therapy are discussed. Unexpectedly, a 2.5-μg once-daily dose of tiotropium (Respimat) had greater efficacy than the 5.0-μg daily dose. Occurrence of a reverse dose response serves to caution us that administering more drug is not always beneficial. Small-airway inflammation contributes to pathogenesis of asthma, especially severe asthma. However, there is no conclusive evidence that the use of small-particle aerosols to target small airways improves clinical outcomes in controlled clinical trials...
May 30, 2017: Respiratory Care
https://www.readbyqxmd.com/read/28546746/genetic-polymorphism-and-chronic-obstructive-pulmonary-disease
#9
REVIEW
Cunhua Yuan, De Chang, Guangming Lu, Xiaowei Deng
Chronic obstructive pulmonary disease (COPD) is a common chronic disease, and its morbidity and mortality are increasing. There are many studies that have tried to explain the pathogenesis of COPD from genetic susceptibility, to identify the susceptibility of COPD factors, which play a role in early prevention, early detection and the early treatment. However, it is well known that COPD is an inflammatory disease characterized by incomplete reversible airflow limitation in which genes interact with the environment...
2017: International Journal of Chronic Obstructive Pulmonary Disease
https://www.readbyqxmd.com/read/28542209/cigarette-smoke-inhibits-lps-induced-fabp5-expression-by-preventing-c-jun-binding-to-the-fabp5-promoter
#10
Deviyani Rao, Anne-Laure Perraud, Carsten Schmitz, Fabienne Gally
Cigarette smoking is the primary cause of chronic obstructive pulmonary disease (COPD) with repeated and sustained infections linked to disease pathogenesis and exacerbations. The airway epithelium constitutes the first line of host defense against infection and is known to be impaired in COPD. We have previously identified Fatty Acid Binding Protein 5 (FABP5) as an important anti-inflammatory player during respiratory infections and showed that overexpression of FABP5 in primary airway epithelial cells protects against bacterial infection and inflammation...
2017: PloS One
https://www.readbyqxmd.com/read/28536707/neutrophilic-inflammation-in-the-immune-responses-of-chronic-obstructive-pulmonary-disease-lessons-from-animal-models
#11
REVIEW
Gang Huang, Xu-Chen Xu, Jie-Sen Zhou, Zhou-Yang Li, Hai-Pin Chen, Yong Wang, Wen Li, Hua-Hao Shen, Zhi-Hua Chen
Chronic obstructive pulmonary disease (COPD) is a major cause of mortality worldwide, which is characterized by chronic bronchitis, destruction of small airways, and enlargement/disorganization of alveoli. It is generally accepted that the neutrophilic airway inflammation observed in the lungs of COPD patients is intrinsically linked to the tissue destruction and alveolar airspace enlargement, leading to disease progression. Animal models play an important role in studying the underlying mechanisms of COPD as they address questions involving integrated whole body responses...
2017: Journal of Immunology Research
https://www.readbyqxmd.com/read/28536249/bronchial-inflammation-and-bacterial-load-in-stable-copd-is-associated-with-tlr4-overexpression
#12
Antonino Di Stefano, Fabio L M Ricciardolo, Gaetano Caramori, Ian M Adcock, Kian Fan Chung, Peter J Barnes, Paola Brun, Andrea Leonardi, Filippo Andò, Davide Vallese, Isabella Gnemmi, Luisella Righi, Francesco Cappello, Bruno Balbi
Toll-like receptors (TLRs) and nucleotide-binding oligomerisation domain (NOD)-like receptors (NLRs) are two major forms of innate immune sensors but their role in the immunopathology of stable chronic obstructive pulmonary disease (COPD) is incompletely studied. Our objective here was to investigate TLR and NLR signalling pathways in the bronchial mucosa in stable COPD.Using immunohistochemistry, the expression levels of TLR2, TLR4, TLR9, NOD1, NOD2, CD14, myeloid differentiation primary response gene 88 (MyD88), Toll-interleukin-1 receptor domain-containing adaptor protein (TIRAP), and the interleukin-1 receptor-associated kinases phospho-IRAK1 and IRAK4 were measured in the bronchial mucosa of subjects with stable COPD of different severity (n=34), control smokers (n=12) and nonsmokers (n=12)...
May 2017: European Respiratory Journal: Official Journal of the European Society for Clinical Respiratory Physiology
https://www.readbyqxmd.com/read/28529637/role-of-the-cxcl8-cxcr1-2-axis-in-cancer-and-inflammatory-diseases
#13
REVIEW
Helen Ha, Bikash Debnath, Nouri Neamati
The chemokine receptors CXCR1/2 and their ligand CXCL8 are essential for the activation and trafficking of inflammatory mediators as well as tumor progression and metastasis. The CXCL8-CXCR1/2 signaling axis is involved in the pathogenesis of several diseases including chronic obstructive pulmonary diseases (COPD), asthma, cystic fibrosis and cancer. Interaction between CXCL8 secreted by select cancer cells and CXCR1/2 in the tumor microenvironment is critical for cancer progression and metastasis. The CXCL8-CXCR1/2 axis may play an important role in tumor progression and metastasis by regulating cancer stem cell (CSC) proliferation and self-renewal...
2017: Theranostics
https://www.readbyqxmd.com/read/28506308/attenuating-immune-pathology-using-a-microbial-based-intervention-in-a-mouse-model-of-cigarette-smoke-induced-lung-inflammation
#14
Mark Bazett, Agnieszka Biala, Ryan D Huff, Matthew R Zeglinksi, Philip M Hansbro, Momir Bosiljcic, Hal Gunn, Shirin Kalyan, Jeremy A Hirota
BACKGROUND: Cigarette smoke exposure is the major risk factor for developing COPD. Presently, available COPD treatments focus on suppressing inflammation and providing bronchodilation. However, these options have varying efficacy in controlling symptoms and do not reverse or limit the progression of COPD. Treatments strategies using bacterial-derived products have shown promise in diseases characterized by inflammation and immune dysfunction. This study investigated for the first time whether a novel immunotherapy produced from inactivated Klebsiella (hereafter referred to as KB) containing all the major Klebsiella macromolecules, could attenuate cigarette smoke exposure-induced immune responses...
May 15, 2017: Respiratory Research
https://www.readbyqxmd.com/read/28502841/use-of-airway-epithelial-cell-culture-to-unravel-the-pathogenesis-and-study-treatment-in-obstructive-airway-diseases
#15
REVIEW
Tinne C J Mertens, Harry Karmouty-Quintana, Christian Taube, Pieter S Hiemstra
Asthma and chronic obstructive pulmonary disease (COPD) are considered as two distinct obstructive diseases. Both chronic diseases share a component of airway epithelial dysfunction. The airway epithelium is localized to deal with inhaled substances, and functions as a barrier preventing penetration of such substances into the body. In addition, the epithelium is involved in the regulation of both innate and adaptive immune responses following inhalation of particles, allergens and pathogens. Through triggering and inducing immune responses, airway epithelial cells contribute to the pathogenesis of both asthma and COPD...
May 11, 2017: Pulmonary Pharmacology & Therapeutics
https://www.readbyqxmd.com/read/28481637/hydrogen-sulfide-a-novel-player-in-airway-development-pathophysiology-of-respiratory-diseases-and-antiviral-defenses
#16
Nikolay Bazhanov, Maria Ansar, Teodora Ivanciuc, Roberto P Garofalo, Antonella Casola
Hydrogen sulfide (H2S) is a biologically relevant signaling molecule in mammals. Together with the volatile substances nitric oxide (NO) and carbon monoxide (CO), H2S is defined as a gasotransmitter, playing a physiological role in a variety of functions such as synaptic transmission, vascular tone, angiogenesis, inflammation and cellular signaling. The generation of H2S is catalyzed by cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE) and 3 mercaptopyruvate sulfurtransferase (3-MST). The expression of CBS and CSE is tissue-specific with CBS being expressed predominantly in the brain and CSE in peripheral tissues, including lungs...
May 8, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28476471/elevated-levels-of-circulating-exosome-in-copd-patients-are-associated-with-systemic-inflammation
#17
Dino B A Tan, Jesse Armitage, Teck-Hui Teo, Nathanael E Ong, Heewoong Shin, Yuben P Moodley
Chronic obstructive pulmonary disease (COPD) is characterized by progressive pulmonary and systemic inflammation. Acute exacerbations of COPD (AECOPD) are associated with acute inflammation and infections and increase the rates of morbidity and mortality. Currently, neither the aetiology nor pathogenesis of AECOPD are entirely understood. Exosomes have been reported to regulate immunity and inflammation via specific intercellular communications through an array of macromolecules (e.g. microRNA and proteins) contained within these microvesicles...
April 26, 2017: Respiratory Medicine
https://www.readbyqxmd.com/read/28458526/mitochondrial-alterations-during-oxidative-stress-in-chronic-obstructive-pulmonary-disease
#18
REVIEW
Ying Jiang, Xiaoqin Wang, Daode Hu
The high incidence of chronic obstructive pulmonary disease (COPD), one of the most prevalent diseases worldwide, has attracted growing attention. Cigarette smoking is considered a major contributory factor in the pathogenesis and progression of COPD due to the tremendous oxidative burden that it causes, which induces an oxidant/antioxidant imbalance. Excessive oxidation induced by the excessive generation of mitochondrial reactive oxygen species disturbs the antioxidant systems and plays an important role in triggering and promoting chronic inflammation of airways...
2017: International Journal of Chronic Obstructive Pulmonary Disease
https://www.readbyqxmd.com/read/28455714/macrophage-dysfunction-in-respiratory-disease
#19
Kylie B R Belchamber, Louise E Donnelly
In the healthy lung, macrophages maintain homeostasis by clearing inhaled particles, bacteria, and removing apoptotic cells from the local pulmonary environment. However, in respiratory diseases including chronic obstructive pulmonary disease (COPD), asthma, and cystic fibrosis, macrophages appear to be dysfunctional and may contribute to disease pathogenesis. In COPD, phagocytosis of bacterial species and apoptotic cells by both alveolar macrophages and monocyte-derived macrophages is significantly reduced, leading to colonization of the lung with pathogenic bacteria...
2017: Results and Problems in Cell Differentiation
https://www.readbyqxmd.com/read/28455454/decrease-in-an-anti-ageing-factor-growth-differentiation-factor-11-in-chronic-obstructive-pulmonary-disease
#20
Katsuhiro Onodera, Hisatoshi Sugiura, Mitsuhiro Yamada, Akira Koarai, Naoya Fujino, Satoru Yanagisawa, Rie Tanaka, Tadahisa Numakura, Shinsaku Togo, Kei Sato, Yorihiko Kyogoku, Yuichiro Hashimoto, Tatsuma Okazaki, Tsutomu Tamada, Seiichi Kobayashi, Masaru Yanai, Motohiko Miura, Yasushi Hoshikawa, Yoshinori Okada, Satoshi Suzuki, Masakazu Ichinose
RATIONALE: Cellular senescence is observed in the lungs of patients with COPD and may contribute to the disease pathogenesis. Growth differentiation factor 11 (GDF11) belongs to the transforming growth factor β superfamily and was recently reported to be a circulating protein that may have rejuvenating effects in mice. We aimed to investigate the amounts of GDF11 in the plasma and the lungs of patients with COPD and elucidate the possible roles of GDF11 in cellular senescence. METHODS: The plasma levels of GDF11 were investigated in two separate cohorts by western blotting...
April 28, 2017: Thorax
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