scholarly journals Transient Ascaris suum larval migration induces intractable chronic pulmonary disease and anemia in mice

2021 ◽  
Vol 15 (12) ◽  
pp. e0010050
Author(s):  
Yifan Wu ◽  
Evan Li ◽  
Morgan Knight ◽  
Grace Adeniyi-Ipadeola ◽  
Li-zhen Song ◽  
...  
Keyword(s):  
Pulmonary Disease ◽  
Lung Diseases ◽  
Pulmonary Hemorrhage ◽  
Lung Damage ◽  
Chronic Obstructive ◽  
Single Episode ◽  
Chronic Anemia ◽  
Larval Migration ◽  
Chronic Lung Diseases

Ascariasis is one of the most common infections in the world and associated with significant global morbidity. Ascaris larval migration through the host’s lungs is essential for larval development but leads to an exaggerated type-2 host immune response manifesting clinically as acute allergic airway disease. However, whether Ascaris larval migration can subsequently lead to chronic lung diseases remains unknown. Here, we demonstrate that a single episode of Ascaris larval migration through lungs induces a chronic pulmonary syndrome of type-2 inflammatory pathology and emphysema accompanied by pulmonary hemorrhage and chronic anemia in a mouse model. Our results reveal that a single episode of Ascaris larval migration through the host lungs leads to permanent lung damage with systemic effects. Remote episodes of ascariasis may drive non-communicable lung diseases such as asthma, chronic obstructive pulmonary disease (COPD), and chronic anemia in parasite endemic regions.

scholarly journals Chronic Obstructive Pulmonary Disease: NHLBI Workshop on the Primary Prevention of Chronic Lung Diseases

2014 ◽  
Vol 11 (Supplement 3) ◽  
pp. S154-S160 ◽  
Author(s):  
M. Bradley Drummond ◽  
A. Sonia Buist ◽  
James D. Crapo ◽  
Robert A. Wise ◽  
Stephen I. Rennard
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Primary Prevention ◽  
Pulmonary Disease ◽  
Lung Diseases ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Chronic Lung Diseases

824 Case Series on the Use of Volume Assured Pressure Support in Patients with Chronic Pulmonary Disease and Progressive Hypercapnia

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A321-A322
Author(s):  
William LeMaster ◽  
Dale Jun ◽  
Sharon De Cruz ◽  
Michelle Zeidler ◽  
Rajan Saggar
Keyword(s):  
Respiratory Failure ◽  
Lung Disease ◽  
Pulmonary Disease ◽  
Lung Diseases ◽  
Lung Transplant ◽  
Pressure Support ◽  
Case Series ◽  
Chronic Obstructive ◽  
Hypoxemic Respiratory Failure ◽  
Chronic Lung Diseases

Abstract Introduction Chronic hypercapnia results from destruction of lung parenchyma which occurs in chronic lung diseases including interstitial lung disease (ILD), bronchiectasis, and chronic lung transplant rejection. Many patients with these diseases will experience progressive respiratory failure eventually requiring consideration of transplantation or re-transplantation. Due to physiologic changes in sleep including reduction in tidal volume, worsening air tapping, and REM atonia, hypoventilation can be exacerbated during the sleeping hours. We present four patients who were prescribed nocturnal Volume Assured Pressure Support VAPS for their progressive hypercapnia. Report of case(s) Subject 1 is a 72 year old female with severe bronchiectasis and restrictive lung disease due to TB pneumonia at a young age. Subject 2 is a 45 year old male with history of pulmonary cavitation due to extensive TB disease when he was younger. Subject 3 is a 45-year-old woman with rheumatoid arthritis related ILD with associated pulmonary arterial hypertension. Subject 4 is a 74 year old patient with a bilateral lung transplant for IPF complicated by bronchiolitis obliterans syndrome who presented with progressive dyspnea and hypercapnia. Despite optimal therapy, all of these patients were admitted for hypercapnic and hypoxemic respiratory failure requiring treatment with BPAP then transitioned to nocturnal VAPS on discharge. For all patients, dyspnea and pCO2 improved as outpatients although all patients did eventually experience an exacerbation of their lung disease requiring repeat admission. Conclusion Due to the physiologic changes that occur with sleep, patients with severe lung disease may experience worsening CO2 retention while sleeping. There is little data assessing the use of chronic nocturnal non-invasive ventilation (NIV) to treat the hypercapnia of chronic lung diseases other than chronic obstructive pulmonary disease, extra-thoracic restriction, and neuromuscular disease. In this case series, nocturnal VAPS stabilized and/or reduced pCO2 in patients with pulmonary parenchymal disease of various etiologies. Additional studies are needed to assess long term effects of VAPS in these patients, including exacerbations, symptoms, and overall mortality. Support (if any):

scholarly journals Hallmarks of the ageing lung

2015 ◽  
Vol 45 (3) ◽  
pp. 807-827 ◽  
Author(s):  
Silke Meiners ◽  
Oliver Eickelberg ◽  
Melanie Königshoff
Keyword(s):  
Lung Cancer ◽  
Chronic Obstructive Pulmonary Disease ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Pulmonary Disease ◽  
Lung Diseases ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Specific Effects ◽  
Chronic Lung Diseases

Ageing is the main risk factor for major non-communicable chronic lung diseases, including chronic obstructive pulmonary disease, most forms of lung cancer and idiopathic pulmonary fibrosis. While the prevalence of these diseases continually increases with age, their respective incidence peaks at different times during the lifespan, suggesting specific effects of ageing on the onset and/or pathogenesis of chronic obstructive pulmonary disease, lung cancer and idiopathic pulmonary fibrosis. Recently, the nine hallmarks of ageing have been defined as cell-autonomous and non-autonomous pathways involved in ageing. Here, we review the available evidence for the involvement of each of these hallmarks in the pathogenesis of chronic obstructive pulmonary disease, lung cancer, or idiopathic pulmonary fibrosis. Importantly, we propose an additional hallmark, “dysregulation of the extracellular matrix”, which we argue acts as a crucial modifier of cell-autonomous changes and functions, and as a key feature of the above-mentioned lung diseases.

scholarly journals The Role of miRNAs in Extracellular Matrix Repair and Chronic Fibrotic Lung Diseases

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1706
Author(s):  
Kauna Usman ◽  
Aileen Hsieh ◽  
Tillie-Louise Hackett
Keyword(s):  
Extracellular Matrix ◽  
Pulmonary Disease ◽  
Lung Diseases ◽  
Cell Function ◽  
Mechanical Stability ◽  
Current Knowledge ◽  
Chronic Obstructive ◽  
Elastic Recoil ◽  
Gene Expressions ◽  
Chronic Lung Diseases

The lung extracellular matrix (ECM) plays a key role in the normal architecture of the lung, from embryonic lung development to mechanical stability and elastic recoil of the breathing adult lung. The lung ECM can modulate the biophysical environment of cells through ECM stiffness, porosity, topography and insolubility. In a reciprocal interaction, lung ECM dynamics result from the synthesis, degradation and organization of ECM components by the surrounding structural and immune cells. Repeated lung injury and repair can trigger a vicious cycle of aberrant ECM protein deposition, accompanied by elevated ECM stiffness, which has a lasting effect on cell and tissue function. The processes governing the resolution of injury repair are regulated by several pathways; however, in chronic lung diseases such as asthma, chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary disease (IPF) these processes are compromised, resulting in impaired cell function and ECM remodeling. Current estimates show that more than 60% of the human coding transcripts are regulated by miRNAs. miRNAs are small non-coding RNAs that regulate gene expressions and modulate cellular functions. This review is focused on the current knowledge of miRNAs in regulating ECM synthesis, degradation and topography by cells and their dysregulation in asthma, COPD and IPF.

scholarly journals Proteases, Mucus, and Mucosal Immunity in Chronic Lung Disease

2021 ◽  
Vol 22 (9) ◽  
pp. 5018
Author(s):  
Michael C. McKelvey ◽  
Ryan Brown ◽  
Sinéad Ryan ◽  
Marcus A. Mall ◽  
Sinéad Weldon ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Lung Disease ◽  
Lung Diseases ◽  
Lung Damage ◽  
Chronic Obstructive ◽  
Lung Function Decline ◽  
Obstructive Pulmonary Disease ◽  
Chronic Lung Diseases ◽  
Multifunctional Enzymes ◽  
Disease Experience

Dysregulated protease activity has long been implicated in the pathogenesis of chronic lung diseases and especially in conditions that display mucus obstruction, such as chronic obstructive pulmonary disease, cystic fibrosis, and non-cystic fibrosis bronchiectasis. However, our appreciation of the roles of proteases in various aspects of such diseases continues to grow. Patients with muco-obstructive lung disease experience progressive spirals of inflammation, mucostasis, airway infection and lung function decline. Some therapies exist for the treatment of these symptoms, but they are unable to halt disease progression and patients may benefit from novel adjunct therapies. In this review, we highlight how proteases act as multifunctional enzymes that are vital for normal airway homeostasis but, when their activity becomes immoderate, also directly contribute to airway dysfunction, and impair the processes that could resolve disease. We focus on how proteases regulate the state of mucus at the airway surface, impair mucociliary clearance and ultimately, promote mucostasis. We discuss how, in parallel, proteases are able to promote an inflammatory environment in the airways by mediating proinflammatory signalling, compromising host defence mechanisms and perpetuating their own proteolytic activity causing structural lung damage. Finally, we discuss some possible reasons for the clinical inefficacy of protease inhibitors to date and propose that, especially in a combination therapy approach, proteases represent attractive therapeutic targets for muco-obstructive lung diseases.

scholarly journals Comorbid Metabolic Disorders in Chronic Lung Diseases

2019 ◽  
pp. 5-15
Author(s):  
M.I. Gumeniuk
Keyword(s):  
Pulmonary Disease ◽  
Metabolic Profile ◽  
Lung Diseases ◽  
Metabolic Disorders ◽  
Specific Treatment ◽  
Chronic Obstructive ◽  
Chronic Pulmonary Disease ◽  
Inflammatory Reactions ◽  
Chronic Lung Diseases ◽  
Pulmonary Pathology

BACKGROUND. Chronic obstructive pulmonary disease (COPD), asthma and interstitial lung diseases (ILD) are often accompanied by various metabolic disorders, aggravating the course and worsening the prognosis of pulmonary pathology. The study of the mechanisms of interaction of systemic inflammatory reactions associated with chronic lung diseases in patients with concomitant metabolic disorders will improve methods for prevention and treatment of complications of this comorbid pathology. MATERIALS AND METHODS. In the PubMed and Google Scholar databases, a literature search has been conducted on the relationship between chronic pulmonary disease and metabolic disorders, as well as the metabolomics of chronic pulmonary disease. RESULTS. Available evidence indicates the role of endocrine system disorders in the pathogenesis of chronic pulmonary pathology. In particular, metabolic concomitant diseases significantly worsen the quality of life of patients and increase mortality. On the other hand, improvement in the metabolic profile in certain categories of patients with chronic lung diseases can positively affect the course of the disease. Preclinical studies indicate the importance of therapeutic recovery of metabolic disorders and the use of circulating metabolites as biomarkers for disease prognosis and treatment response. CONCLUSIONS. Monitoring of metabolic parameters, in particular glucose, lipids, thyroid hormones, calcium and vitamin D, should be a part of everyday clinical practice in all patients with COPD, asthma and ILD. Prescribing specific treatment based on the patient’s metabolic profile can slow progression and reduce mortality in chronic lung diseases.

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