scholarly journals Age- and airway disease related gene expression patterns of key SARS-CoV-2 entry factors in human nasal epithelia

2021 ◽  
Author(s):  
Mihkel Plaas ◽  
Kadri Seppa ◽  
Nayana Gaur ◽  
Priit Kasenomm ◽  
Mario Plaas
Keyword(s):  
Gene Expression ◽  
Expression Patterns ◽  
Inverse Correlation ◽  
The Elderly ◽  
Airway Disease ◽  
Disease Course ◽  
Significant Inverse Correlation ◽  
Chronic Airway Disease ◽  
Patient Groups ◽  
Disease Related Gene

The global COVID-19 pandemic caused by SARS-CoV-2 predominantly affects the elderly. Differential expression of SARS-CoV-2 entry genes may underlie the variable susceptibility in different patient groups. Here, we examined the gene expression of key SARS-CoV-2 entry factors in mucosal biopsies to delineate the roles of age and existing chronic airway disease. A significant inverse correlation between ACE2 and age and a downregulation of NRP1 in patients with airway disease were noted. These results indicate that the interplay between various factors may influence susceptibility and the disease course.

scholarly journals Cryopreservation of microglia enables single-cell RNA sequencing with minimal effects on disease-related gene expression patterns

iScience ◽  
2021 ◽  
Vol 24 (4) ◽  
pp. 102357
Author(s):  
Brenda Morsey ◽  
Meng Niu ◽  
Shetty Ravi Dyavar ◽  
Courtney V. Fletcher ◽  
Benjamin G. Lamberty ◽  
...  
Keyword(s):  
Gene Expression ◽  
Single Cell ◽  
Rna Sequencing ◽  
Expression Patterns ◽  
Gene Expression Patterns ◽  
Related Gene ◽  
Single Cell Rna Sequencing ◽  
Disease Related Gene

scholarly journals A changing signaling environment induces multiciliated cell trans-differentiation during developmental remodeling

2020 ◽  
Author(s):  
Alexia Tasca ◽  
Martin Helmstädter ◽  
Magdalena Brislinger ◽  
Maximilian Haas ◽  
Peter Walentek
Keyword(s):  
Gene Expression ◽  
Tissue Remodeling ◽  
Airway Disease ◽  
Secretory Cells ◽  
Basal Bodies ◽  
Lysosomal Degradation ◽  
Developmental Mechanism ◽  
Multiciliated Cells ◽  
Chronic Airway Disease ◽  
Developmental Remodeling

AbstractMulticiliated cells (MCCs) are extremely highly-differentiated, presenting >100 cilia and basal bodies. We analyzed how MCCs are lost from the airway-like Xenopus embryonic epidermis during developmental tissue remodeling. We found that some MCCs undergo apoptosis, but that the majority trans-differentiate into secretory cells. Trans-differentiation involves loss of ciliary gene expression, cilia retraction and lysosomal degradation. Apoptosis and trans-differentiation are both induced by a changing signaling environment through Notch, Jak/STAT, Thyroid hormone and mTOR signaling, and trans-differentiation can be inhibited by Rapamycin. This demonstrates that even cells with extreme differentiation features can undergo direct fate conversion. Our data further suggest that the reactivation of this developmental mechanism in adults can drive tissue remodeling in human chronic airway disease, a paradigm resembling cancer formation and progression.

Gene expression profiling in inflammatory airway disease associated with elevated adenosine

2002 ◽  
Vol 282 (2) ◽  
pp. L169-L182 ◽  
Author(s):  
Suman K. Banerjee ◽  
Hays W. J. Young ◽  
Jonathan B. Volmer ◽  
Michael R. Blackburn
Keyword(s):  
Gene Expression ◽  
Molecular Mechanisms ◽  
Expression Patterns ◽  
Cdna Array ◽  
Airway Disease ◽  
Lung Damage ◽  
In Vivo Model ◽  
Mouse Cdna ◽  
Deficient Mice

Adenosine has been implicated as a modulator of inflammatory processes central to asthma. However, the molecular mechanisms involved are poorly understood. We used Atlas mouse cDNA arrays to analyze differential gene expression in association with lung inflammation resulting from elevated adenosine in adenosine deaminase (ADA)-deficient mice. We report that of the 1,176 genes on the array, the expression patterns of 280 genes were consistently altered. Of these genes, the steady-state levels of 93 genes were upregulated and 29 were downregulated. We also show that lowering adenosine levels with ADA enzyme therapy has striking effects on gene expression that may be associated with resolution of pulmonary eosinophilia. In addition, we confirmed the nucleic acid and protein expression of vascular endothelial growth factor and monocyte chemoattractant protein-3, two candidate genes that may be regulated by adenosine. In conclusion, high-throughput profiling of gene expression by cDNA array hybridization has provided an overview of critical regulatory genes involved in airway inflammation in ADA-deficient mice. These mice will serve as a useful in vivo model for characterizing molecular mechanisms of adenosine-mediated lung damage.

scholarly journals The nasopharyngeal microbiome

2017 ◽  
Vol 1 (4) ◽  
pp. 297-312 ◽  
Author(s):  
David W. Cleary ◽  
Stuart C. Clarke
Keyword(s):  
Respiratory Tract ◽  
The Elderly ◽  
Airway Disease ◽  
Invasive Disease ◽  
Microbial Consortia ◽  
Environmental Drivers ◽  
Respiratory Morbidity ◽  
Future Research ◽  
Upper Respiratory Tract ◽  
Chronic Airway Disease

Human microbiomes have received increasing attention over the last 10 years, leading to a pervasiveness of hypotheses relating dysbiosis to health and disease. The respiratory tract has received much less attention in this respect than that of, for example, the human gut. Nevertheless, progress has been made in elucidating the immunological, ecological and environmental drivers that govern these microbial consortia and the potential consequences of aberrant microbiomes. In this review, we consider the microbiome of the nasopharynx, a specific niche of the upper respiratory tract. The nasopharynx is an important site, anatomically with respect to its gateway position between upper and lower airways, and for pathogenic bacterial colonisation. The dynamics of the latter are important for long-term respiratory morbidity, acute infections of both invasive and non-invasive disease and associations with chronic airway disease exacerbations. Here, we review the development of the nasopharyngeal (NP) microbiome over the life course, examining it from the early establishment of resilient profiles in neonates through to perturbations associated with pneumonia risk in the elderly. We focus specifically on the commensal, opportunistically pathogenic members of the NP microbiome that includes Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae and Moraxella catarrhalis. In addition, we consider the role of relatively harmless genera such as Dolosigranulum and Corynebacterium. Understanding that the NP microbiome plays such a key, beneficial role in maintaining equilibrium of commensal species, prevention of pathogen outgrowth and host immunity enables future research to be directed appropriately.

scholarly journals Consistent Biomarkers and Related Pathogenesis Underlying Asthma Revealed by Systems Biology Approach

2019 ◽  
Vol 20 (16) ◽  
pp. 4037 ◽  
Author(s):  
Xiner Nie ◽  
Jinyi Wei ◽  
Youjin Hao ◽  
Jingxin Tao ◽  
Yinghong Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Molecular Mechanisms ◽  
Expression Patterns ◽  
Interaction Network ◽  
Bronchial Epithelium ◽  
Airway Disease ◽  
Arachidonic Acid Metabolism ◽  
Functional Enrichment ◽  
Chemical Stimulus ◽  
Extracellular Region

Asthma is a common chronic airway disease worldwide. Due to its clinical and genetic heterogeneity, the cellular and molecular processes in asthma are highly complex and relatively unknown. To discover novel biomarkers and the molecular mechanisms underlying asthma, several studies have been conducted by focusing on gene expression patterns in epithelium through microarray analysis. However, few robust specific biomarkers were identified and some inconsistent results were observed. Therefore, it is imperative to conduct a robust analysis to solve these problems. Herein, an integrated gene expression analysis of ten independent, publicly available microarray data of bronchial epithelial cells from 348 asthmatic patients and 208 healthy controls was performed. As a result, 78 up- and 75 down-regulated genes were identified in bronchial epithelium of asthmatics. Comprehensive functional enrichment and pathway analysis revealed that response to chemical stimulus, extracellular region, pathways in cancer, and arachidonic acid metabolism were the four most significantly enriched terms. In the protein-protein interaction network, three main communities associated with cytoskeleton, response to lipid, and regulation of response to stimulus were established, and the most highly ranked 6 hub genes (up-regulated CD44, KRT6A, CEACAM5, SERPINB2, and down-regulated LTF and MUC5B) were identified and should be considered as new biomarkers. Pathway cross-talk analysis highlights that signaling pathways mediated by IL-4/13 and transcription factor HIF-1α and FOXA1 play crucial roles in the pathogenesis of asthma. Interestingly, three chemicals, polyphenol catechin, antibiotic lomefloxacin, and natural alkaloid boldine, were predicted and may be potential drugs for asthma treatment. Taken together, our findings shed new light on the common molecular pathogenesis mechanisms of asthma and provide theoretical support for further clinical therapeutic studies.

Gene expression patterns in blood predict future severe endpoints in community acquired pneumonia

Pneumologie ◽  
2018 ◽  
Vol 72 (S 01) ◽  
pp. S8-S9
Author(s):  
M Bauer ◽  
H Kirsten ◽  
E Grunow ◽  
P Ahnert ◽  
M Kiehntopf ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Patterns ◽  
Community Acquired Pneumonia ◽  
Gene Expression Patterns

High Levels of Plasma Protein C in Nephrotic Syndrome

1985 ◽  
Vol 53 (01) ◽  
pp. 005-007 ◽  
Author(s):  
I Pabinger-Fasching ◽  
K Lechner ◽  
H Niessner ◽  
P Schmidt ◽  
E Balzar ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Plasma Protein ◽  
Protein C ◽  
Inverse Correlation ◽  
Elevated Plasma ◽  
Significant Inverse Correlation ◽  
At Iii ◽  
Thrombotic Tendency ◽  
Protein C Activity

SummaryIn patients with severe nephrotic syndrome determinations of plasma protein C : Ag levels (8 patients: 5 adults, 3 children) and protein C activity (3 out of 8 patients) revealed significantly elevated plasma protein C concentrations. Furthermore we observed a significant inverse correlation of protein C : Ag to AT III : Ag levels. No protein C : Ag could be detected in the urine of two patients studied. We conclude from our data, that changes of plasma protein C do not contribute to the high thrombotic tendency in nephrotic syndrome.

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