scholarly journals Association of Rhinovirus Infections with Asthma

1999 ◽  
Vol 12 (1) ◽  
pp. 9-18 ◽  
Author(s):  
James E. Gern ◽  
William W. Busse
Keyword(s):  
Allergic Inflammation ◽  
Epidemiologic Studies ◽  
Detection Methods ◽  
Chronic Obstructive ◽  
Tissue Destruction ◽  
Obstructive Pulmonary Disease ◽  
Antiviral Responses ◽  
Asthma Exacerbations ◽  
Rhinovirus Infection ◽  
The Common

SUMMARY Rhinoviruses are the most common cause of the common cold, but they can cause more severe illnesses in people with underlying lung disorders such as asthma, chronic obstructive pulmonary disease, or cystic fibrosis. Epidemiologic studies with sensitive detection methods such as PCR have identified rhinovirus infection as a major source of asthma exacerbations in both children and adults, especially during the spring and fall. Since rhinoviruses cause little tissue destruction, it is presumed that the immune response to the infection may play an important role in the pathogenesis of rhinovirus-induced exacerbations of asthma. This review examines the epidemiologic association between rhinovirus infections and exacerbations of asthma and outlines current information on immune responses to rhinovirus infection and potential connections between antiviral responses and preexisting allergic inflammation. Finally, current and future strategies for treating rhinovirus infections and virus-induced exacerbations of asthma are discussed.

scholarly journals Orchestration of Neutrophil Extracellular Traps (Nets), a Unique Innate Immune Function during Chronic Obstructive Pulmonary Disease (COPD) Development

Biomedicines ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 53
Author(s):  
Anjali Trivedi ◽  
Meraj A. Khan ◽  
Geetanjali Bade ◽  
Anjana Talwar
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Neutrophil Extracellular Traps ◽  
Innate Immune ◽  
Chronic Obstructive ◽  
Tissue Destruction ◽  
Mucus Production ◽  
Obstructive Pulmonary Disease ◽  
Extracellular Traps ◽  
Endothelial Cell Death

Morbidity, mortality and economic burden caused by chronic obstructive pulmonary disease (COPD) is a significant global concern. Surprisingly, COPD is already the third leading cause of death worldwide, something that WHO had not predicted to occur until 2030. It is characterized by persistent respiratory symptoms and airway limitation due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles of gases. Neutrophil is one of the key infiltrated innate immune cells in the lung during the pathogenesis of COPD. Neutrophils during pathogenic attack or injury decide to undergo for a suicidal death by releasing decondensed chromatin entangled with antimicrobial peptides to trap and ensnare pathogens. Casting neutrophil extracellular traps (NETs) has been widely demonstrated to be an effective mechanism against invading microorganisms thus controlling overwhelming infections. However, aberrant and massive NETs formation has been reported in several pulmonary diseases, including chronic obstructive pulmonary disease. Moreover, NETs can directly induce epithelial and endothelial cell death resulting in impairing pulmonary function and accelerating the progression of the disease. Therefore, understanding the regulatory mechanism of NET formation is the need of the hour in order to use NETs for beneficial purpose and controlling their involvement in disease exacerbation. For example, DNA neutralization of NET proteins using protease inhibitors and disintegration with recombinant human DNase would be helpful in controlling excess NETs. Targeting CXC chemokine receptor 2 (CXCR2) would also reduce neutrophilic inflammation, mucus production and neutrophil-proteinase mediated tissue destruction in lung. In this review, we discuss the interplay of NETs in the development and pathophysiology of COPD and how these NETs associated therapies could be leveraged to disrupt NETopathic inflammation as observed in COPD, for better management of the disease.

scholarly journals COVID-19 Shuts Doors to Flu but Keeps Them Open to Rhinoviruses

Biology ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 733
Author(s):  
Irina Kiseleva ◽  
Andrey Ksenafontov
Keyword(s):  
Influenza Pandemic ◽  
Age Groups ◽  
Influenza Viruses ◽  
Interferon Response ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Mild Disease ◽  
Viral Interference ◽  
The Common

It is well known that rhinoviruses are distributed across the globe and are the most common cause of the common cold in all age groups. Rhinoviruses are widely considered to be harmless because they are generally perceived as respiratory viruses only capable of causing mild disease. However, they may also infect the lower respiratory tract, inducing chronic obstructive pulmonary disease and exacerbations of asthma, bronchiolitis, etc. The role of rhinoviruses in pathogenesis and the epidemiological process is underestimated, and they need to be intensively studied. In the light of recent data, it is now known that rhinoviruses could be one of the key epidemiological barriers that may influence the spread of influenza and novel coronaviruses. It has been reported that endemic human rhinoviruses delayed the development of the H1N1pdm09 influenza pandemic through viral interference. Moreover, human rhinoviruses have been suggested to block SARS-CoV-2 replication in the airways by triggering an interferon response. In this review, we summarized the main biological characteristics of genetically distinct viruses such as rhinoviruses, influenza viruses, and SARS-CoV-2 in an attempt to illuminate their main discrepancies and similarities. We hope that this comparative analysis will help us to better understand in which direction research in this area should move.

scholarly journals A NEW PERSPECTIVE ON BRONCHIAL ASTHMA AND CHRONIC OBSTRUCTIVE PULMONARY DISEASE OVERLAP: POTENTIAL DIAGNOSTIC CRITERIA

2020 ◽  
Vol 73 (7) ◽  
pp. 1480-1483
Author(s):  
Tetyana O. Pertseva ◽  
Lyudmyla I. Konopkina ◽  
Alina O. Babenko
Keyword(s):  
Allergic Inflammation ◽  
Chronic Obstructive ◽  
Bronchial Obstruction ◽  
Obstructive Pulmonary Disease ◽  
Total Ige ◽  
Copd Patients ◽  
Group 2 ◽  
New Perspective ◽  
High Level ◽  
Blood Eosinophils

The aim: The aim of the research was to analyze the results of observation and examination of COPD patients in order to identify a group of individuals with potential asthma overlap. Materials and methods: We have conducted a two-stage dynamic investigation of 43 COPD patients during 3–8 years. The patients were divided into two groups: group 1 counted 30 individuals who presented with at least one episode of reversible bronchial obstruction (RBO) during the observation; group 2 – 13 individuals who presented with nonreversible bronchial obstruction (nonRBO). At the first stage, we conducted a clinical observations analysis and studied lung function examination records; at the second stage, we calculated the markers of allergic inflammation. Results: It was revealed that around 70% of COPD patients have occasional episodes of RBO. It was established that the level of blood eosinophils in these patients on the whole is rather low even in people with intermittent RBO, and the total IgE level appeared to be significantly higher in patients with intermittent RBO comparing to the level of this marker in patients who have nonRBO. Conclusions: COPD patients with intermittent RBO and high level of total IgE level form a group with potential asthma overlap.

Clinical Profile of Critically Ill Patients Presenting to Emergency Department of Tertiary Level Hospital of Nepal

2019 ◽  
Vol 41 (1) ◽  
pp. 67-74
Author(s):  
Shubha K Shrestha ◽  
Bishwas Pradhan ◽  
Yogendra M Shakya ◽  
Hem R Paneru
Keyword(s):  
Critically Ill ◽  
Critically Ill Patients ◽  
University Teaching ◽  
Chronic Obstructive ◽  
Optimal Care ◽  
Obstructive Pulmonary Disease ◽  
Number Of Patients ◽  
Common Diagnosis ◽  
The Common ◽  
A Prospective Study

Introduction: Among critically ill patients presenting to Emergency Room (ER) of Tribhuwan University Teaching Hospital (TUTH), a number of patients have to either remain in ER or have to be referred outside due to unavailability of critical care beds. Studies have shown significant association between delayed admission and mortality rates along with increased length of stay and higher cost. This study aimed to present an audit of critically ill patients presenting to ER of TUTH. Methods: This was a prospective study conducted over a period of one month. All patients presenting to ER of TUTH were triaged and critically ill patients were shifted to Red area of the ER. All patients ≥16 years of age shifted to Red area during the study period were enrolled in our study. Results: Out of 3718 patients presenting to ER during the study period, the number of critically ill patients ≥16 years of age was 526 i.e. 14.14% of total patients. Among them, the common diagnosis were Cerebrovascular Accidents (CVA) followed by Intoxication, Acute Exacerbation (AE) of Chronic Obstructive Pulmonary Disease (COPD), Pneumonia and Chronic Kidney Disease (CKD) respectively. Almost 20% of these patients were admitted, 31% were referred and 40% were shifted for observation. The median length of ER stay was 6 hours (Mean: 8.5 hrs; Range: 20 min to 70 hr 15 min). Conclusion: Among critically ill patients presenting to our ER, almost 1/5th of the patients were admitted whereas more than 2/3rd were either referred or remained in our ER. This data highlights the need for solutions to provide optimal care for the acute phase management of the critically ill patients.

Paradoxical effects of mild hypoxia and moderate altitude on human visual perception

1992 ◽  
Vol 83 (5) ◽  
pp. 633-636 ◽  
Author(s):  
Thomas E. Schlaepfer ◽  
Peter Bärtsch ◽  
Hans U. Fisch
Keyword(s):  
Cognitive Performance ◽  
Chronic Obstructive ◽  
Moderate Altitude ◽  
Human Visual Perception ◽  
Obstructive Pulmonary Disease ◽  
Hypoxic Conditions ◽  
Paradoxical Effects ◽  
Common Notion ◽  
The Common ◽  
Mild Hypoxia

1. Prolonged (> 10h) exposure to hypoxia and high altitude (> 5000 m) invariably have detrimental effects on cognitive performance. Paradoxically, mild improvements in cognitive function in patients with chronic obstructive pulmonary disease after cessation of oxygen therapy have been reported. 2. We studied in each of 10 healthy subjects the effect of an acute altitude challenge [rapid helicopter transport to the Jungfraujoch (3450 m), experiment 1] and of an acute exposure to mild hypoxia (fractional inspiratory oxygen concentration 14.5%, experiment 2) on a simple test of cognitive performance (the time needed to read briefly displayed letters). 3. Under both hypoxic conditions the time needed to read briefly presented letters decreased, from 12.1 ± sd 3.8 ms to 8.3 ± 1.5 ms (P<0.01) in experiment 1, and from 11.9 ± 1.9 ms to 8.1 ± 1.1 ms (P<0.01) in experiment 2. 4. A rapid and mild hypoxic challenge seems to improve a simple measure of cognitive performance above normal values. The common notion that exposure to hypoxia and altitude invariably impairs cognitive performance may have to be re-evaluated.

scholarly journals IL-17C contributes to NTHi-induced inflammation and lung damage in experimental COPD and is present in sputum during acute exacerbations

PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0243484
Author(s):  
Giovanna Vella ◽  
Felix Ritzmann ◽  
Lisa Wolf ◽  
Andreas Kamyschnikov ◽  
Hannah Stodden ◽  
...  
Keyword(s):  
Disease Severity ◽  
Lung Inflammation ◽  
Pulmonary Inflammation ◽  
Airway Epithelial Cells ◽  
Lung Damage ◽  
Chronic Obstructive ◽  
Tissue Destruction ◽  
Obstructive Pulmonary Disease ◽  
Neutrophilic Inflammation ◽  
Acute Exacerbations

Neutrophilic inflammation results in loss of lung function in chronic obstructive pulmonary disease (COPD). Gram-negative bacteria, such as nontypeable Haemophilus influenzae (NTHi), trigger acute exacerbations of COPD (AECOPD) and contribute to chronic lung inflammation. The pro-inflammatory cytokine interleukin-17C (IL-17C) is expressed by airway epithelial cells and regulates neutrophilic chemotaxis. Here, we explored the function of IL-17C in NTHi- and cigarette smoke (CS)-induced models of COPD. Neutrophilic inflammation and tissue destruction were decreased in lungs of IL-17C-deficient mice (Il-17c-/-) chronically exposed to NTHi. Numbers of pulmonary neutrophils were decreased in Il-17c-/- mice after acute exposure to the combination of NTHi and CS. However, Il-17c-/- mice were not protected from CS-induced lung inflammation. In a preliminary patient study, we show that IL-17C is present in sputum samples obtained during AECOPD and associates with disease severity. Concentrations of IL-17C were significantly increased during advanced COPD (GOLD III/IV) compared to moderate COPD (GOLD I/II). Concentrations of IL-17A and IL-17E did not associate with disease severity. Our data suggest that IL-17C promotes harmful pulmonary inflammation triggered by bacteria in COPD.

scholarly journals Role of Type2 Inflammatory Biomarkers in Chronic Obstructive Pulmonary Disease

2020 ◽  
Vol 9 (8) ◽  
pp. 2670
Author(s):  
Keiji Oishi ◽  
Kazuto Matsunaga ◽  
Toshihiro Shirai ◽  
Keita Hirai ◽  
Yasuhiro Gon
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Stable State ◽  
Epidemiologic Studies ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Blood Eosinophils ◽  
The Relationship

Airway inflammation in chronic obstructive pulmonary disease (COPD) is typically thought to be driven by Type1 immune responses, while Type2 inflammation appears to be present in definite proportions in the stable state and during exacerbations. In fact, some COPD patients showed gene expression of Type2 inflammation in the airway, and this subset was associated with the inhaled corticosteroid (ICS) response. Interestingly enough, the relationship between COPD and diseases associated with Type2 inflammation from the perspective of impaired lung development is increasingly highlighted by recent epidemiologic studies on the origin of COPD. Therefore, many researchers have shown an interest in the prevalence and the role of existent Type2 biomarkers such as sputum and blood eosinophils, exhaled nitric oxide fraction, and atopy, not only in asthma but also in COPD. Although the evidence about Type2 biomarkers in COPD is inconsistent and less robust, Type2 biomarkers have shown some potential when analyzing various clinical outcomes or therapeutic response to ICS. In this article, we review the existent and emerging Type2 biomarkers with clinically higher applicability in the management of COPD.

scholarly journals Lung Macrophage Functional Properties in Chronic Obstructive Pulmonary Disease

2020 ◽  
Vol 21 (3) ◽  
pp. 853 ◽  
Author(s):  
Kentaro Akata ◽  
Stephan F. van Eeden
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Inflammatory Response ◽  
Pulmonary Disease ◽  
Cigarette Smoke ◽  
Functional Properties ◽  
Chronic Obstructive ◽  
Tissue Destruction ◽  
Obstructive Pulmonary Disease ◽  
Chronic Inflammatory Response ◽  
Immune Effector

Chronic obstructive pulmonary disease (COPD) is caused by the chronic exposure of the lungs to toxic particles and gases. These exposures initiate a persistent innate and adaptive immune inflammatory response in the airways and lung tissues. Lung macrophages (LMs) are key innate immune effector cells that identify, engulf, and destroy pathogens and process inhaled particles, including cigarette smoke and particulate matter (PM), the main environmental triggers for COPD. The number of LMs in lung tissues and airspaces is increased in COPD, suggesting a potential key role for LMs in initiating and perpetuating the chronic inflammatory response that underpins the progressive nature of COPD. The purpose of this brief review is to discuss the origins of LMs, their functional properties (chemotaxis, recruitment, mediator production, phagocytosis and apoptosis) and changes in these properties due to exposure to cigarette smoke, ambient particulate and pathogens, as well as their persistent altered functional properties in subjects with established COPD. We also explore the potential to therapeutically modulate and restore LMs functional properties, to improve impaired immune system, prevent the progression of lung tissue destruction, and improve both morbidity and mortality related to COPD.

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