scholarly journals Rhinovirus-Induced Exacerbations of Asthma and COPD

Scientifica ◽  
2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Marc B. Hershenson

Over the past two decades, increasing evidence has shown that, in patients with chronic airways disease, viral infection is the most common cause of exacerbation. This review will examine the evidence for viral-induced exacerbations of asthma and chronic obstructive lung disease and the potential mechanisms by which viruses cause exacerbations. Attention will be focused on rhinovirus, the most common cause of respiratory exacerbations. Exacerbations due to rhinovirus, which infects relatively few cells in the airway and does not cause the cytotoxicity of other viruses such as influenza or respiratory syncytial virus, are particularly poorly understood. While the innate immune response likely plays a role in rhinovirus-induced exacerbations, its precise role, either adaptive or maladaptive, is debated. Because current treatment strategies are only partially effective, further research examining the cellular and molecular mechanisms underlying viral-induced exacerbations of chronic airways diseases is warranted.

Author(s):  
Diane Moujalled ◽  
Andreas Strasser ◽  
Jeffrey R. Liddell

AbstractTightly orchestrated programmed cell death (PCD) signalling events occur during normal neuronal development in a spatially and temporally restricted manner to establish the neural architecture and shaping the CNS. Abnormalities in PCD signalling cascades, such as apoptosis, necroptosis, pyroptosis, ferroptosis, and cell death associated with autophagy as well as in unprogrammed necrosis can be observed in the pathogenesis of various neurological diseases. These cell deaths can be activated in response to various forms of cellular stress (exerted by intracellular or extracellular stimuli) and inflammatory processes. Aberrant activation of PCD pathways is a common feature in neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS), Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease, resulting in unwanted loss of neuronal cells and function. Conversely, inactivation of PCD is thought to contribute to the development of brain cancers and to impact their response to therapy. For many neurodegenerative diseases and brain cancers current treatment strategies have only modest effect, engendering the need for investigations into the origins of these diseases. With many diseases of the brain displaying aberrations in PCD pathways, it appears that agents that can either inhibit or induce PCD may be critical components of future therapeutic strategies. The development of such therapies will have to be guided by preclinical studies in animal models that faithfully mimic the human disease. In this review, we briefly describe PCD and unprogrammed cell death processes and the roles they play in contributing to neurodegenerative diseases or tumorigenesis in the brain. We also discuss the interplay between distinct cell death signalling cascades and disease pathogenesis and describe pharmacological agents targeting key players in the cell death signalling pathways that have progressed through to clinical trials.


2006 ◽  
Vol 134 (6) ◽  
pp. 1174-1178 ◽  
Author(s):  
R. E. G. UPSHUR ◽  
R. MOINEDDIN ◽  
E. J. CRIGHTON ◽  
M. MAMDANI

Co-circulation of respiratory syncytial virus (RSV) and influenza has made the partitioning of morbidity and mortality from each virus difficult. Given the interaction between chronic obstructive lung disease (COPD) and pneumonia, often one can be mistaken for the other. Multivariate time-series methodology was applied to examine the impact of RSV and influenza on hospital admissions for bronchiolitis, pneumonia, and COPD. The Granger Causality Test, used to determine the causal relationship among series, showed that COPD and pneumonia are not influenced by RSV (P=0·2999 and 0·7725), but RSV does influence bronchiolitis (P=0·0001). Influenza was found to influence COPD, pneumonia, and bronchiolitis (P<0·0001). The use of multivariate time series and Granger causality applied to epidemiological data clearly illustrates the significant contribution of influenza and RSV to morbidity in the population.


Medicina ◽  
2018 ◽  
Vol 54 (5) ◽  
pp. 72 ◽  
Author(s):  
Lina Jankauskaitė ◽  
Valdonė Misevičienė ◽  
Laimutė Vaidelienė ◽  
Rimantas Kėvalas

Studies of human airway virome are relatively recent and still very limited. Culture-independent microbial techniques showed growing evidence of numerous viral communities in the respiratory microbial ecosystem. The significance of different acute respiratory viruses is already known in the pathogenesis of chronic conditions, such as asthma, cystic fibrosis (CF), or chronic obstructive lung disease (COPD), and their exacerbations. Viral pathogens, such as influenza, metapneumovirus, parainfluenza, respiratory syncytial virus, or rhinovirus, have been associated with impaired immune response, acute exacerbations, and decrease in lung function in chronic lung diseases. However, more data have attributed a role to Herpes family viruses or the newly identified Anelloviridae family of viruses in chronic diseases, such as asthma, idiopathic pulmonary fibrosis (IPF), or CF. Impaired antiviral immunity, bacterial colonization, or used medication, such as glucocorticoids or antibiotics, contribute to the imbalance of airway microbiome and may shape the local viral ecosystem. A specific part of virome, bacteriophages, frames lung microbial communities through direct contact with its host, the specific bacteria known as Pseudomonas aeruginosa or their biofilm formation. Moreover, antibiotic resistance is induced through phages via horizontal transfer and leads to more severe exacerbations of chronic airway conditions. Morbidity and mortality of asthma, COPD, CF, and IPF remains high, despite an increased understanding and knowledge about the impact of respiratory virome in the pathogenesis of these conditions. Thus, more studies focus on new prophylactic methods or therapeutic agents directed toward viral–host interaction, microbial metabolic function, or lung microbial composition rearrangement.


2019 ◽  
Vol 20 (10) ◽  
pp. 2557 ◽  
Author(s):  
Yuichiro Ukon ◽  
Takahiro Makino ◽  
Joe Kodama ◽  
Hiroyuki Tsukazaki ◽  
Daisuke Tateiwa ◽  
...  

Osteoporosis is an unavoidable public health problem in an aging or aged society. Anti-resorptive agents (calcitonin, estrogen, and selective estrogen-receptor modulators, bisphosphonates, anti-receptor activator of nuclear factor κB ligand antibody along with calcium and vitamin D supplementations) and anabolic agents (parathyroid hormone and related peptide analogs, sclerostin inhibitors) have major roles in current treatment regimens and are used alone or in combination based on the pathological condition. Recent advancements in the molecular understanding of bone metabolism and in bioengineering will open the door to future treatment paradigms for osteoporosis, including antibody agents, stem cells, and gene therapies. This review provides an overview of the molecular mechanisms, clinical evidence, and potential adverse effects of drugs that are currently used or under development for the treatment of osteoporosis to aid clinicians in deciding how to select the best treatment option.


2020 ◽  
Vol 21 (18) ◽  
pp. 6924
Author(s):  
Molly Easter ◽  
Seth Bollenbecker ◽  
Jarrod W. Barnes ◽  
Stefanie Krick

Chronic obstructive pulmonary disease (COPD) has become a global epidemic and is the third leading cause of death worldwide. COPD is characterized by chronic airway inflammation, loss of alveolar-capillary units, and progressive decline in lung function. Major risk factors for COPD are cigarette smoking and aging. COPD-associated pathomechanisms include multiple aging pathways such as telomere attrition, epigenetic alterations, altered nutrient sensing, mitochondrial dysfunction, cell senescence, stem cell exhaustion and chronic inflammation. In this review, we will highlight the current literature that focuses on the role of age and aging-associated signaling pathways as well as their impact on current treatment strategies in the pathogenesis of COPD. Furthermore, we will discuss established and experimental COPD treatments including senolytic and anti-aging therapies and their potential use as novel treatment strategies in COPD.


2016 ◽  
Vol 43 (11) ◽  
pp. 1956-1964 ◽  
Author(s):  
Sigrun R. Hofmann ◽  
Anja Schnabel ◽  
Angela Rösen-Wolff ◽  
Henner Morbach ◽  
Hermann J. Girschick ◽  
...  

Chronic nonbacterial osteomyelitis (CNO) is an autoinflammatory bone disorder, covering a clinical spectrum with asymptomatic inflammation of single bones at the one end, and chronic recurrent multifocal osteomyelitis (CRMO) at the other end. The exact molecular pathophysiology of CNO remains largely unknown. Provided familial clusters and the association with inflammatory disorders of the skin and intestine suggest a genetic predisposition. Recently, profound dysregulation of cytokine responses was demonstrated in CRMO. Failure to produce antiinflammatory cytokines interleukin (IL)-10 and IL-19 contributes to activation of inflammasomes and subsequent IL-1β release. In IL-10–deficient and in CNO-prone chronic multifocal osteomyelitis mice, IL-1β was linked to bone inflammation. Further, alterations to the gut microbiome were suggested in contributing to IL-1β release from innate immune cells in mice, offering an interesting target in the search for molecular mechanisms in CNO. Here, we summarize clinical presentation and treatment options in CNO/CRMO, current pathophysiological concepts, available mouse models, and promising future scientific directions.


2020 ◽  
Author(s):  
Denis Seyres ◽  
Alessandra Cabassi ◽  
John J Lambourne ◽  
Frances Burden ◽  
Samantha Farrow ◽  
...  

AbstractThe molecular characterisation of the cardiometabolic syndrome could improve our understanding of its pathogenesis and pathophysiology and guide the identification of new treatment strategies. We identified the combinations of features that help to define the cardiometabolic syndrome using a multi-omic penalised logistic regression approach, from in-depth phenotyping, including transcriptome and epigenome profiling of innate immune cells, platelets, plasma metabolomics and extensive biochemistry, of 202 blood donors and two groups with extreme phenotypes (obese and lipodystrophy). This allowed us to determine the likelihood of the individuals in the donor group of having an increased cardio-metabolic risk and to determine the molecular mechanisms at play. To investigate if the observed effects were reversible, we repeated the in-depth phenotyping six months after bariatric surgery. These analyses revealed patterns of abnormal activation in innate immunity cells in the extreme phenotype groups, which were abrogated after surgery with the establishment of new gene expression landscapes.


2020 ◽  
Vol 28 ◽  
pp. 204020662094730
Author(s):  
Elena Margret Thornhill ◽  
Jessica Salpor ◽  
David Verhoeven

Respiratory Syncytial Virus is a yearly respiratory virus that causes significant frequencies of morbidities, particularly in the young and elderly populations. However, preventive vaccines and/or treatment therapies are generally lacking, although much attention is now being placed on this virus. Moreover, there are now multiple strategies currently being explored in a race to the first licensed vaccine. While vaccines are being developed, multiple treatment strategies are being explored to attenuate the severity of infection and thus reduce hospitalization rates in vulnerable populations. This review outlines current strategies to prevent or treat this virus in the hopes of reducing significant human morbidity and mortality that occurs yearly with this seasonal virus.


VASA ◽  
2012 ◽  
Vol 41 (5) ◽  
pp. 313-318 ◽  
Author(s):  
Ernemann ◽  
Bender ◽  
Melms ◽  
Brechtel ◽  
Kobba ◽  
...  

Interventional therapies using angioplasty and stenting of symptomatic stenosis of the proximal supraaortic vessels have evolved as safe and effective treatment strategies. The aim of this paper is to summarize the current treatment concepts for stenosis in the subclavian and brachiocephalic artery with regard to clinical indication, interventional technique including selection of the appropriate vascular approach and type of stent, angiographic and clinical short-term and long-term results and follow-up. The role of hybrid interventions for tandem stenoses of the carotid bifurcation and brachiocephalic artery is analysed. A systematic review of data for angioplasty and stenting of symptomatic extracranial vertebral artery stenosis is discussed with a special focus on restenosis rate.


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