scholarly journals The role of microRNAs in chronic respiratory disease: recent insights

2018 ◽  
Vol 399 (3) ◽  
pp. 219-234 ◽  
Author(s):  
Lindsay R. Stolzenburg ◽  
Ann Harris
Keyword(s):  
Respiratory Disease ◽  
Inflammatory Cells ◽  
Chronic Respiratory Disease ◽  
Chronic Obstructive ◽  
Lung Pathology ◽  
Obstructive Pulmonary Disease ◽  
Chronic Respiratory Diseases ◽  
And Function ◽  
Mirna Abundance

AbstractChronic respiratory diseases encompass a group of diverse conditions affecting the airways, which all impair lung function over time. They include cystic fibrosis (CF), idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD) and asthma, which together affect hundreds of millions of people worldwide. MicroRNAs (miRNAs), a class of small non-coding RNAs involved in post-transcriptional gene repression, are now recognized as major regulators in the development and progression of chronic lung disease. Alterations in miRNA abundance occur in lung tissue, inflammatory cells, and freely circulating in blood and are thought to function both as drivers and modifiers of disease. Their importance in lung pathology has prompted the development of miRNA-based therapies and biomarker tools. Here, we review the current literature on miRNA expression and function in chronic respiratory disease and highlight further research that is needed to propel miRNA treatments for lung disorders towards the clinic.

The Role of Epithelial-Mesenchymal Transition in Chronic Obstructive Pulmonary Disease

2017 ◽  
Vol 203 (2) ◽  
pp. 99-104 ◽  
Author(s):  
Jo-Maree Courtney ◽  
Patricia L. Spafford
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Respiratory Disease ◽  
Epithelial Mesenchymal Transition ◽  
Chronic Respiratory Disease ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Mesenchymal Transition ◽  
Potential Benefits

Chronic obstructive pulmonary disease (COPD) is a major cause of mortality worldwide, and there is currently no treatment that can halt the progression of the disease. Over the last decade there has been increasing interest in the idea that epithelial-mesenchymal transition (EMT) may be active in COPD. Here we review the evidence for EMT in COPD as well as the current progress being made on understanding the drivers and mechanisms involved. Finally, we discuss the potential benefits that understanding EMT may bring to the field of chronic respiratory disease.

scholarly journals Immunoproteasomes as a novel antiviral mechanism in rhinovirus-infected airways

2018 ◽  
Vol 132 (15) ◽  
pp. 1711-1723 ◽  
Author(s):  
Kris Genelyn Dimasuay ◽  
Amelia Sanchez ◽  
Niccolette Schaefer ◽  
Jorge Polanco ◽  
Deborah A. Ferrington ◽  
...  
Keyword(s):  
Viral Load ◽  
Antigen Processing ◽  
Lower Airway ◽  
Chronic Obstructive ◽  
Deficient Mouse ◽  
Obstructive Pulmonary Disease ◽  
Tracheal Epithelial Cells ◽  
And Function

Rhinovirus (RV) infection is involved in acute exacerbations of asthma and chronic obstructive pulmonary disease (COPD). RV primarily infects upper and lower airway epithelium. Immunoproteasomes (IP) are proteolytic machineries with multiple functions including the regulation of MHC class I antigen processing during viral infection. However, the role of IP in RV infection has not been explored. We sought to investigate the expression and function of IP during airway RV infection. Primary human tracheobronchial epithelial (HTBE) cells were cultured at air–liquid interface (ALI) and treated with RV16, RV1B, or interferon (IFN)-λ in the absence or presence of an IP inhibitor (ONX-0914). IP gene (i.e. LMP2) deficient mouse tracheal epithelial cells (mTECs) were cultured for the mechanistic studies. LMP2-deficient mouse model was used to define the in vivo role of IP in RV infection. IP subunits LMP2 and LMP7, antiviral genes MX1 and OAS1 and viral load were measured. Both RV16 and RV1B significantly increased the expression of LMP2 and LMP7 mRNA and proteins, and IFN-λ mRNA in HTBE cells. ONX-0914 down-regulated MX1 and OAS1, and increased RV16 load in HTBE cells. LMP2-deficient mTECs showed a significant increase in RV1B load compared with the wild-type (WT) cells. LMP2-deficient (compared with WT) mice increased viral load and neutrophils in bronchoalveolar lavage (BAL) fluid after 24 h of RV1B infection. Mechanistically, IFN-λ induction by RV infection contributed to LMP2 and LMP7 up-regulation in HTBE cells. Our data suggest that IP are induced during airway RV infection, which in turn may serve as an antiviral and anti-inflammatory mechanism.

scholarly journals Characteristics and Role of Neutrophil Extracellular Traps in Asthma

Inflammation ◽  
2021 ◽  
Author(s):  
Fei Chen ◽  
Min Yu ◽  
Yonghong Zhong ◽  
Lina Wang ◽  
Huaqiong Huang
Keyword(s):  
Systematic Review ◽  
Protective Effect ◽  
Allergic Asthma ◽  
Respiratory Disease ◽  
Bronchial Asthma ◽  
Inflammatory Cells ◽  
Neutrophil Extracellular Traps ◽  
Chronic Respiratory Disease ◽  
Extracellular Traps

Abstract Asthma is a common chronic respiratory disease that affects millions of people worldwide. The incidence of asthma has continued to increase every year. Bronchial asthma involves a variety of cells, including airway inflammatory cells, structural cells, and neutrophils, which have gained more attention because they secrete substances that play an important role in the occurrence and development of asthma. Neutrophil extracellular traps (NETs) are mesh-like structures composed of DNA, histones, and non-histone molecules that can be secreted from neutrophils. NETs can enrich anti-bacterial substances and limit pathogen migration, thus having a protective effect in case of inflammation. However, despite of their anti-inflammatory properties, NETs have been shown to trigger allergic asthma and worsen asthma progression. Here, we provide a systematic review of the roles of NETs in asthma.

scholarly journals High Frequency of Viral Co-Detections in Acute Bronchiolitis

Viruses ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 990
Author(s):  
Hortense Petat ◽  
Vincent Gajdos ◽  
François Angoulvant ◽  
Pierre-Olivier Vidalain ◽  
Sandrine Corbet ◽  
...  
Keyword(s):  
Respiratory Diseases ◽  
Virus Detection ◽  
Public Health Issue ◽  
Chronic Obstructive ◽  
Acute Bronchiolitis ◽  
Obstructive Pulmonary Disease ◽  
Chronic Respiratory Diseases ◽  
Coronavirus Infection ◽  
Syncytial Virus

Over two years (2012–2014), 719 nasopharyngeal samples were collected from 6-week- to 12-month-old infants presenting at the emergency department with moderate to severe acute bronchiolitis. Viral testing was performed, and we found that 98% of samples were positive, including 90% for respiratory syncytial virus, 34% for human rhino virus, and 55% for viral co-detections, with a predominance of RSV/HRV co-infections (30%). Interestingly, we found that the risk of being infected by HRV is higher in the absence of RSV, suggesting interferences or exclusion mechanisms between these two viruses. Conversely, coronavirus infection had no impact on the likelihood of co-infection involving HRV and RSV. Bronchiolitis is the leading cause of hospitalizations in infants before 12 months of age, and many questions about its role in later chronic respiratory diseases (asthma and chronic obstructive pulmonary disease) exist. The role of virus detection and the burden of viral codetections need to be further explored, in order to understand the physiopathology of chronic respiratory diseases, a major public health issue.

scholarly journals Dysregulation of the glutaredoxin/S-glutathionylation redox axis in lung diseases

2020 ◽  
Vol 318 (2) ◽  
pp. C304-C327 ◽  
Author(s):  
Shi B. Chia ◽  
Evan A. Elko ◽  
Reem Aboushousha ◽  
Allison M. Manuel ◽  
Cheryl van de Wetering ◽  
...  
Keyword(s):  
Lung Diseases ◽  
Defense Mechanism ◽  
Protein S ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Mixed Disulfide ◽  
Glutathione S Transferases ◽  
And Function ◽  
Redox Buffer

Glutathione is a major redox buffer, reaching millimolar concentrations within cells and high micromolar concentrations in airways. While glutathione has been traditionally known as an antioxidant defense mechanism that protects the lung tissue from oxidative stress, glutathione more recently has become recognized for its ability to become covalently conjugated to reactive cysteines within proteins, a modification known as S-glutathionylation (or S-glutathiolation or protein mixed disulfide). S-glutathionylation has the potential to change the structure and function of the target protein, owing to its size (the addition of three amino acids) and charge (glutamic acid). S-glutathionylation also protects proteins from irreversible oxidation, allowing them to be enzymatically regenerated. Numerous enzymes have been identified to catalyze the glutathionylation/deglutathionylation reactions, including glutathione S-transferases and glutaredoxins. Although protein S-glutathionylation has been implicated in numerous biological processes, S-glutathionylated proteomes have largely remained unknown. In this paper, we focus on the pathways that regulate GSH homeostasis, S-glutathionylated proteins, and glutaredoxins, and we review methods required toward identification of glutathionylated proteomes. Finally, we present the latest findings on the role of glutathionylation/glutaredoxins in various lung diseases: idiopathic pulmonary fibrosis, asthma, and chronic obstructive pulmonary disease.

scholarly journals Microbiota: A Missing Link in The Pathogenesis of Chronic Lung Inflammatory Diseases

2021 ◽  
Vol 70 (1) ◽  
pp. 25-32
Author(s):  
AGNIESZKA MAGRYŚ
Keyword(s):  
Respiratory Diseases ◽  
Inflammatory Diseases ◽  
Chronic Obstructive ◽  
High Morbidity ◽  
Obstructive Pulmonary Disease ◽  
Chronic Respiratory Diseases ◽  
Chronic Pulmonary Diseases ◽  
Underlying Mechanisms

Chronic respiratory diseases account for high morbidity and mortality, with asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis (CF) being the most prevalent globally. Even though the diseases increase in prevalence, the exact underlying mechanisms have still not been fully understood. Despite their differences in nature, pathophysiologies, and clinical phenotypes, a growing body of evidence indicates that the presence of lung microbiota can shape the pathogenic processes underlying chronic inflammation, typically observed in the course of the diseases. Therefore, the characterization of the lung microbiota may shed new light on the pathogenesis of these diseases. Specifically, in chronic respiratory tract diseases, the human microbiota may contribute to the disease’s development and severity. The present review explores the role of the microbiota in the area of chronic pulmonary diseases, especially COPD, asthma, and CF.

scholarly journals Cigarette Smoke Suppresses the Surface Expression ofc-kitand FcεRI on Mast Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
M. E. Givi ◽  
B. R. Blokhuis ◽  
C. A. Da Silva ◽  
I. Adcock ◽  
J. Garssen ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mast Cells ◽  
Cigarette Smoke ◽  
Inflammatory Cells ◽  
Surface Expression ◽  
Chronic Obstructive ◽  
Independent Manner ◽  
Obstructive Pulmonary Disease ◽  
Short Term Exposure ◽  
And Function

Chronic obstructive pulmonary disease (COPD) is a multicomponent disease characterized by emphysema and/or chronic bronchitis. COPD is mostly associated with cigarette smoking. Cigarette smoke contains over 4,700 chemical compounds, including free radicals and LPS (a Toll-Like Receptor 4 agonist) at concentrations which may contribute to the pathogenesis of diseases like COPD. We have previously shown that short-term exposure to cigarette smoke medium (CSM) can stimulate several inflammatory cells via TLR4 and that CSM reduces the degranulation of bone-marrow-derived mast cells (BMMCs). In the current study, the effect of CSM on mast cells maturation and function was investigated. Coculturing of BMMC with CSM during the development of bone marrow progenitor cells suppressed the granularity and the surface expression ofc-kitand FcεRI receptors. Stimulation with IgE/antigen resulted in decreased degranulation and release of Th1 and Th2 cytokines. The effects of CSM exposure could not be mimicked by the addition of LPS to the culture medium. In conclusion, this study shows that CSM may affect mast cell development and subsequent response to allergic activation in a TLR4-independent manner.

scholarly journals Infection-Associated Mechanisms of Neuro-Inflammation and Neuro-Immune Crosstalk in Chronic Respiratory Diseases

2021 ◽  
Vol 22 (11) ◽  
pp. 5699
Author(s):  
Belinda Camp ◽  
Sabine Stegemann-Koniszewski ◽  
Jens Schreiber
Keyword(s):  
Respiratory Diseases ◽  
Respiratory Infections ◽  
Airflow Obstruction ◽  
Microbial Colonization ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Chronic Respiratory Diseases ◽  
Neuro Inflammation

Chronic obstructive airway diseases are characterized by airflow obstruction and airflow limitation as well as chronic airway inflammation. Especially bronchial asthma and chronic obstructive pulmonary disease (COPD) cause considerable morbidity and mortality worldwide, can be difficult to treat, and ultimately lack cures. While there are substantial knowledge gaps with respect to disease pathophysiology, our awareness of the role of neurological and neuro-immunological processes in the development of symptoms, the progression, and the outcome of these chronic obstructive respiratory diseases, is growing. Likewise, the role of pathogenic and colonizing microorganisms of the respiratory tract in the development and manifestation of asthma and COPD is increasingly appreciated. However, their role remains poorly understood with respect to the underlying mechanisms. Common bacteria and viruses causing respiratory infections and exacerbations of chronic obstructive respiratory diseases have also been implicated to affect the local neuro-immune crosstalk. In this review, we provide an overview of previously described neuro-immune interactions in asthma, COPD, and respiratory infections that support the hypothesis of a neuro-immunological component in the interplay between chronic obstructive respiratory diseases, respiratory infections, and respiratory microbial colonization.

scholarly journals The potential protective role of corticosteroid therapy in patients with asthma and COPD against COVID-19

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Fabiana Furci ◽  
Marco Caminati ◽  
Gianenrico Senna ◽  
Sebastiano Gangemi
Keyword(s):  
Corticosteroid Therapy ◽  
Positive Outcome ◽  
Chronic Respiratory Disease ◽  
Protective Role ◽  
Chronic Obstructive ◽  
Main Body ◽  
Obstructive Pulmonary Disease ◽  
Asthmatic Patients ◽  
Chronic Lung Diseases

Abstract Background The observation of patients hospitalized for coronavirus disease (COVID-19) led us to note a lower prevalence of patients affected by chronic respiratory disease, in particular asthmatic patients, compared to the general population. Therefore, the aim of this paper is to evaluate the possible protective role of corticosteroid therapy in patients with chronic lung disease, regarding the risk of contracting severe COVID-19. Main body SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) receptors to enter the cells. Considering the high number of these receptors in patients affected by asthma and chronic obstructive pulmonary disease (COPD), the evidence that these patients do not have a high risk of hospitalization for COVID-19 needs further study to understand what the possible protective “factors” are in these patients. In particular, the finding in some studies of reduced coronavirus replication in cell lines treated with steroids, molecules commonly used for treating chronic lung diseases, needs further attention. Short conclusion The hypothesis that corticosteroids, commonly used in treating airways diseases, might modify the severity of SARS-CoV-2 disease has become a key point and a possible predictive factor of a positive outcome of COVID-19 in patients treated everyday with these molecules.

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