scholarly journals The Heterogeneity of Inflammatory Response and Emphysema in Chronic Obstructive Pulmonary Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Xia Xu ◽  
Ke Huang ◽  
Fen Dong ◽  
Shiwei Qumu ◽  
Qichao Zhao ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Inflammatory Response ◽  
Airway Inflammation ◽  
Pulmonary Disease ◽  
Airway Remodeling ◽  
Neutrophil Infiltration ◽  
Airway Disease ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Alveolar Septa

Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease characterized by chronic inflammation, emphysema, airway remodeling, and altered lung function. Despite the canonical classification of COPD as a neutrophilic disease, blood and airway eosinophilia are found in COPD patients. Identifying the tools to assess eosinophilic airway inflammation in COPD models during stable disease and exacerbations will enable the development of novel anti-eosinophilic treatments. We developed different animal models to mimic the pathological features of COPD. Our results show that eosinophils accumulated in the lungs of pancreatic porcine elastase-treated mice, with emphysema arising from the alveolar septa. A lipopolysaccharide challenge significantly increased IL-17 levels and induced a swift change from a type-2 response to an IL-17-driven inflammatory response. However, lipopolysaccharides can exacerbate cigarette smoking-induced airway inflammation dominated by neutrophil infiltration and airway remodeling in COPD models. Our results suggest that eosinophils may be associated with emphysema arising from the alveolar septa, which may be different from the small airway disease-associated emphysema that is dominated by neutrophilic inflammation in cigarette smoke-induced models. The characterization of heterogeneity seen in the COPD-associated inflammatory signature could pave the way for personalized medicine to identify new and effective therapeutic approaches for COPD.

scholarly journals “Targeted Therapy in Eosinophilic Chronic Obstructive Pulmonary Disease”

2021 ◽  
pp. 00437-2020
Author(s):  
Mathieu Fieldes ◽  
Chloé Bourguignon ◽  
Said Assou ◽  
Amel Nasri ◽  
Aurélie Fort ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Airway Inflammation ◽  
Pulmonary Disease ◽  
Public Health Problem ◽  
Airway Disease ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Lung Function Decline ◽  
Eosinophilic Asthma ◽  
Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is a common and preventable airway disease causing significant worldwide mortality and morbidity. Lifetime exposure to tobacco smoking and environmental particles are the two major risk factors. Over the last decades, COPD has become a growing public health problem with an increase in incidence. COPD is defined by airflow limitation due to airway inflammation and small airway remodelling coupled to parenchymal lung destruction. Most patients exhibit neutrophil-predominant airway inflammation combined with an increase in macrophages and CD8+ T-cells. Asthma is a heterogeneous chronic inflammatory airway disease. The most studied subtypes is T2 high eosinophilic asthma, for which there are an increasing number of biologic agents developed. However, both asthma and COPD are complex and share common pathophysiologic mechanisms. They are known as overlapping syndromes as approximately 40% of patients with COPD present an eosinophilic airway inflammation. Several studies suggest a putative role of eosinophilia in lung function decline and COPD exacerbation. Recently, pharmacological agents targeting eosinophilic traits in uncontrolled eosinophilic asthma, especially monoclonal antibodies directed against interleukins (IL5, IL4, IL13) or their receptors, have shown promising results. This review examines data on the rationale for such biological agents and assesses efficacy in T2-endotype COPD patients.

scholarly journals Chronic Obstructive Pulmonary Disease (COPD) and Asthma-Chronic Obstructive Pulmonary Disease Overlap Syndrome (ACOS) are Risk Factors for Cryptococcosis

2020 ◽  
Vol 11 (1) ◽  
pp. 1-4
Author(s):  
Aline B. Mahler Pereira ◽  
Alexandre P. Rogerio
Keyword(s):  
Risk Factors ◽  
Chronic Obstructive Pulmonary Disease ◽  
Immune Response ◽  
Airway Inflammation ◽  
Pulmonary Disease ◽  
Airway Remodeling ◽  
Overlap Syndrome ◽  
Chronic Obstructive ◽  
Host Immune System ◽  
Obstructive Pulmonary Disease

Cryptococcosis is a fungal infection of global importance affecting the central nervous system and other organs such as the lungs. The severity of cryptococcosis is largely dependent on the integrity of the host immune system. The protection to cryptococcosis is associated with Th1 immune response while Th2 results in susceptibility to Cryptococcus infection. Asthma is a chronic inflammatory disease commonly coordinated by Th2 immune response. The airway inflammation in Chronic Obstructive Pulmonary Disease (COPD) patients is characterized by increased neutrophils, macrophages, proteases, IL-6, IL-8, and Th1 cytokines. Asthma-Chronic Obstructive Pulmonary Disease Overlap Syndrome (ACOS) patients present phenotype that shares Th1 (COPD) and Th2 (asthma). There are several risk factors associated with Cryptococcus infection, including smoking, that cause airway remodeling and dysregulated and damaging airway inflammation.

The role of gene polymorphisms in the pathogenesis of chronic obstructive pulmonary disease

Biologia ◽  
2008 ◽  
Vol 63 (1) ◽  
Author(s):  
Eva Slabá ◽  
Pavol Joppa ◽  
Ján Šalagovič ◽  
Ružena Tkáčová
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Inflammatory Response ◽  
Candidate Genes ◽  
Pulmonary Disease ◽  
Gene Polymorphisms ◽  
Association Studies ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Positional Candidate ◽  
Linkage Analyses

AbstractChronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide. Irreversible airflow limitation, both progressive and associated with an inflammatory response of the lungs to noxious particles or gases, is a hallmark of the disease. Cigarette smoking is the most important environmental risk factor for COPD, nevertheless, only approximately 20–30% of smokers develop symptomatic disease. Epidemiological studies, case-control studies in relatives of patients with COPD, and twin studies suggest that COPD is a genetically complex disease with environmental factors and many involved genes interacting together. Two major strategies have been employed to identify the genes and the polymorphisms that likely contribute to the development of complex diseases: association studies and linkage analyses. Biologically plausible pathogenetic mechanisms are prerequisites to focus the search for genes of known function in association studies. Protease-antiprotease imbalance, generation of oxidative stress, and chronic inflammation are recognized as the principal mechanisms leading to irreversible airflow obstruction and parenchymal destruction in the lung. Therefore, genes which have been implicated in the pathogenesis of COPD are involved in antiproteolysis, antioxidant barrier and metabolism of xenobiotic substances, inflammatory response to cigarette smoke, airway hyperresponsiveness, and pulmonary vascular remodelling. Significant associations with COPD-related phenotypes have been reported for polymorphisms in genes coding for matrix metalloproteinases, microsomal epoxide hydrolase, glutathione-S-transferases, heme oxygenase, tumor necrosis factor, interleukines 1, 8, and 13, vitamin D-binding protein and β-2-adrenergic receptor (ADRB2), whereas adequately powered replication studies failed to confirm most of the previously observed associations. Genome-wide linkage analyses provide us with a novel tool to identify the general locations of COPD susceptibility genes, and should be followed by association analyses of positional candidate genes from COPD pathophysiology, positional candidate genes selected from gene expression studies, or dense single nucleotide polymorphism panels across regions of linkage. Haplotype analyses of genes with multiple polymorphic sites in linkage disequilibrium, such as the ADRB2 gene, provide another promising field that has yet to be explored in patients with COPD. In the present article we review the current knowledge about gene polymorphisms that have been recently linked to the risk of developing COPD and/or may account for variations in the disease course.

The role of beta-agonist therapy for chronic obstructive airway disease in patients with coexistent atrial fibrillation: Literature review

2021 ◽  
Vol 2 (6) ◽  
Author(s):  
Rodríguez Miguel ◽  
◽  
Chinta Siddharth ◽  
Vittorio Timothy ◽  
◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Airway Disease ◽  
The Other ◽  
Beta Agonist ◽  
Beta Blockade ◽  
Chronic Obstructive ◽  
Agonist Therapy ◽  
Obstructive Pulmonary Disease

Background: New advances have been made in medicine, but the incidence and prevalence of Chronic Obstructive Pulmonary Disease (COPD) are evident, and it is established as the fourth cause of death in the United States representing a high cost for the healthcare system. This condition has been related to atrial fibrillation due to the changes in the lungs and vasculature. Based on this history, we seek to evaluate the outcome of AF in the patients with COPD and its relationship with medical therapy utilized to treat this pulmonary condition with the objective of establishing the relationship between the use of beta-agonist therapy for obstructive airway disease in patients with AF. Discussion: Cell receptors participate in multiple reactions and the sympathetic response is received via the alpha- and beta-receptors are related to the hemodynamic of the vasculature of the lungs and cardiovascular system. The beta-blockade agents are one of the most common medication classes used for rate control in cardiac arrhythmias, but the side effect could be COPD exacerbation; on the other hand, beta-adrenergic or beta-agonist as a therapy for this pulmonary condition could increase the heart rate leading to AF decompensation. There is a clear dilemma in our patients who have airway disease and AF since the treatment for one might worsen the other. The clear benefit in morbidity and mortality of beta-blocker therapy, especially beta1-selective, outweighs the potential for any pulmonary side-effects related to ex-acerbation of COPD or airway disease. Conclusion: There is clear data showing the evidence of the potential paradoxical side-effect between COPD and AF therapies, given the exacerbation of one due to treatment of the other, benefits versus risks should be discussed and the medical decision should be made based on them. The deteriorated cardiac condition can rapidly predispose to critical complications leading to death, which is why the use of beta-blockade agents will be chosen over possible complications with pulmonary disease. In other words, the benefit should outweigh the risk based on the best outcome for the patient. Keywords: atrial fibrillation; pulmonary disease; obstructive pulmonary disease; chronic obstructive pulmonary disease (COPD); B-Agonist; B-Block (selective; non-selective); digitalis; other antiarrhythmic.

scholarly journals Characterization of the inflammatory response to inhaled lipopolysaccharide in mild to moderate chronic obstructive pulmonary disease

2015 ◽  
Vol 79 (5) ◽  
pp. 767-776 ◽  
Author(s):  
Vandana Gupta ◽  
Antonia Banyard ◽  
Aoibheann Mullan ◽  
Srividya Sriskantharajah ◽  
Thomas Southworth ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Inflammatory Response ◽  
Pulmonary Disease ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease
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