scholarly journals Abnormal Airway Mucus Secretion Induced by Virus Infection

2021 ◽  
Vol 12 ◽  
Author(s):  
Yao Li ◽  
Xiao Xiao Tang
Keyword(s):  
Virus Infection ◽  
Respiratory Viruses ◽  
Mucus Secretion ◽  
Structural Components ◽  
Mucus Hypersecretion ◽  
Research Advance ◽  
Airway Mucus ◽  
Mucus Barrier ◽  
Human Airways ◽  
Underlying Mechanisms

The airway mucus barrier is a primary defensive layer at the airway surface. Mucins are the major structural components of airway mucus that protect the respiratory tract. Respiratory viruses invade human airways and often induce abnormal mucin overproduction and airway mucus secretion, leading to airway obstruction and disease. The mechanism underlying the virus-induced abnormal airway mucus secretion has not been fully studied so far. Understanding the mechanisms by which viruses induce airway mucus hypersecretion may open new avenues to treatment. In this article, we elaborate the clinical and experimental evidence that respiratory viruses cause abnormal airway mucus secretion, review the underlying mechanisms, and also discuss the current research advance as well as potential strategies to treat the abnormal airway mucus secretion caused by SARS-CoV-2.

scholarly journals Brg1 Promotes Airway Mucus Hypersecretion via IL-13 and the JAK1/2-STAT6 Signaling Pathway in Asthma

2022 ◽  
Author(s):  
Wenjing Zou ◽  
maozhu xu ◽  
Jie Hu ◽  
Lili Yang ◽  
Gang Gen ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Signaling Pathway ◽  
Periodic Acid ◽  
Airway Epithelial Cells ◽  
Mucus Secretion ◽  
Control Group ◽  
Airway Epithelial ◽  
Wild Type ◽  
Mucus Hypersecretion ◽  
Airway Mucus

Abstract Backgroud: The chromatin remodeling factor Brg1 (Brahma-related gene 1) is an important nuclear protein that promotes the transcriptional activation or inhibition of target genes by regulating ATP hydrolysis to generate energy which rearranges the position of nucleosomes and the interaction of histone DNA. In this study, we explored the effect of Brg1 on airway mucus hypersecretion in asthma.Methods: Six-to-eight-week-old female wild-type C57BL/6 mice (wild-type, WT) and type II alveolar epithelial cells (AECIIs) specifically knockout Brg1 mice (Brg1fl/fl) were selected as the experimental subjects. The asthma group was established with house dust mite (HDM), and the control group was treated with normal saline (n=10). Wright's staining was used to detect inflammatory cells in bronchoalveolar lavage fluid (BALF). Invasive lung function was used to assess the airway compliance. Hematoxylin and eosin and periodic acid-schiff staining were used to detect mucus secretion. The virus was used to knock down the Brg1 gene in the bronchial epithelial cell line (16HBE) and stimulated with HDM. Immunohistochemistry was used to measure mucin glycoprotein 5AC (MUC5AC) protein expression in the airway epithelium and 16HBE cells. Western blotting was used to detect the expression of the MUC5AC and JAK1/2-STAT6 signaling pathways in mouse lung tissue and 16HBE. Co-immunoprecipitation (Co-IP) and Chromatin Immunoprecipitation (CHIP) were used to detect whether Brg1 could regulate the JAK1/2-STAT6 signaling pathway.Results: Specifically, knocking out the Brg1 gene in AECIIs can reduce airway inflammation, airway compliance, and mucus hypersecretion in asthma. Knockdown of the Brg1 gene can simultaneously reduce Interleukin-13 (IL-13) and the expression of MUC5AC protein in airway epithelial cells and the activation of the JAK1/2-STAT6 signaling pathway. The results of Co-IP and CHIP showed that Brg1 could bind to the JAK1/2 promoter region, regulating the activity of the JAK1/2-STAT6 pathway affects airway mucus secretion in asthma.Conclusion: Brg1 gene knockout in airway epithelial cells can reduce asthmatic airway mucus hypersecretion and the expression of MUC5AC protein in airway epithelial cells partly by inhibiting the activation of the JAK1/2-STAT6 signaling pathway.

scholarly journals IFITM3 protects the heart during influenza virus infection

2019 ◽  
Author(s):  
Adam D. Kenney ◽  
Temet M. McMichael ◽  
Alexander Imas ◽  
Nicholas M. Chesarino ◽  
Lizhi Zhang ◽  
...  
Keyword(s):  
Heart Rate ◽  
Influenza Virus ◽  
Virus Infection ◽  
Cardiac Dysfunction ◽  
Influenza A ◽  
Transmembrane Protein ◽  
Influenza Virus Infection ◽  
Small Animal ◽  
Heart Tissue ◽  
Underlying Mechanisms

AbstractInfluenza virus primarily targets the lungs, but dissemination and damage to heart tissue is also known to occur in severe infections. Despite this knowledge, influenza virus-induced cardiac pathogenesis and its underlying mechanisms have been difficult to study due to a lack of small animal models. In humans, polymorphisms in the gene encoding interferon-induced transmembrane protein 3 (IFITM3), an antiviral restriction factor, are associated with susceptibility to severe influenza, but whether IFITM3 deficiencies contribute to other aspects of pathogenesis, including cardiac dysfunction, is unknown. We now show that IFITM3 deficiency in a newly generated knockout (KO) mouse model exacerbates illness and mortality following influenza A virus infection. Enhanced pathogenesis correlated with increased replication of virus in the lungs, spleens, and hearts of KO mice relative to wildtype (WT) mice. IFITM3 KO mice exhibited normal cardiac function at baseline, but developed severely aberrant electrical activity upon infection, including decreased heart rate and irregular, arrhythmic RR (interbeat) intervals. In contrast, WT mice exhibited a mild decrease in heart rate without irregularity of RR intervals. Heightened cardiac virus titers and electrical dysfunction in KO animals was accompanied by increased activation of fibrotic pathways and fibrotic lesions in the heart. Our findings reveal an essential role for IFITM3 in controlling influenza virus replication and pathogenesis in heart tissue and establish IFITM3 KO mice as a powerful model to study virus-induced cardiac dysfunction.

scholarly journals Management and Therapy for Airway Mucus Hypersecretion

2012 ◽  
Vol 101 (12) ◽  
pp. 3525-3532 ◽  
Author(s):  
Mitsuko Kondo ◽  
Jun Tamaoki
Keyword(s):  
Mucus Hypersecretion ◽  
Airway Mucus

scholarly journals In vivo culture models of airway mucus hypersecretion

1996 ◽  
Vol 71 ◽  
pp. 28
Author(s):  
Yoshiaki Inayama ◽  
Satoshi Asano ◽  
Masayoshi Kanisawa
Keyword(s):  
Mucus Hypersecretion ◽  
In Vivo Culture ◽  
Culture Models ◽  
Airway Mucus

scholarly journals PPARγas a Potential Target to Treat Airway Mucus Hypersecretion in Chronic Airway Inflammatory Diseases

PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Yongchun Shen ◽  
Lei Chen ◽  
Tao Wang ◽  
Fuqiang Wen
Keyword(s):  
Transcription Factor ◽  
Inflammatory Diseases ◽  
Chronic Obstructive ◽  
Peroxisome Proliferator ◽  
Mucus Hypersecretion ◽  
Mucin Production ◽  
Airway Mucus ◽  
Chronic Airway

Airway mucus hypersecretion (AMH) is a key pathophysiological feature of chronic airway inflammatory diseases such as bronchial asthma, cystic fibrosis, and chronic obstructive pulmonary disease. AMH contributes to the pathogenesis of chronic airway inflammatory diseases, and it is associated with reduced lung function and high rates of hospitalization and mortality. It has been suggested that AMH should be a target in the treatment of chronic airway inflammatory diseases. Recent evidence suggests that a key regulator of airway inflammation, hyperresponsiveness, and remodeling is peroxisome proliferator-activated receptor gamma (PPARγ), a ligand-activated transcription factor that regulates adipocyte differentiation and lipid metabolism. PPARγis expressed in structural, immune, and inflammatory cells in the lung. PPARγis involved in mucin production, and PPARγagonists can inhibit mucin synthesis bothin vitroandin vivo. These findings suggest that PPARγis a novel target in the treatment of AMH and that further work on this transcription factor may lead to new therapies for chronic airway inflammatory diseases.

Influence of coexistence of mild OSA on airway mucus hypersecretion in patients with COPD

2020 ◽  
Author(s):  
Nansheng Wan ◽  
Xin Tang ◽  
Hui Ding ◽  
Yuxia Yan ◽  
Yan Zhuang ◽  
...  
Keyword(s):  
Mucus Hypersecretion ◽  
Airway Mucus

scholarly journals The Potential Role and Regulatory Mechanisms of MUC5AC in Chronic Obstructive Pulmonary Disease

Molecules ◽  
2020 ◽  
Vol 25 (19) ◽  
pp. 4437 ◽  
Author(s):  
Jingyuan Li ◽  
Zuguang Ye
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Signaling Pathways ◽  
Pulmonary Disease ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Chronic Obstructive ◽  
High Morbidity ◽  
Obstructive Pulmonary Disease ◽  
Mucus Hypersecretion ◽  
Airway Mucus

Chronic obstructive pulmonary disease (COPD) is associated with high morbidity and mortality globally. Studies show that airway mucus hypersecretion strongly compromises lung function, leading to frequent hospitalization and mortality, highlighting an urgent need for effective COPD treatments. MUC5AC is known to contribute to severe muco-obstructive lung diseases, worsening COPD pathogenesis. Various pathways are implicated in the aberrant MUC5AC production and secretion MUC5AC. These include signaling pathways associated with mucus-secreting cell differentiation [nuclear factor-κB (NF-κB)and IL-13-STAT6- SAM pointed domain containing E26 transformation-specific transcription factor (SPDEF), as well as epithelial sodium channel (ENaC) and cystic fibrosis transmembrane conductance regulator (CFTR)], and signaling pathways related to mucus transport and excretion-ciliary beat frequency (CBF). Various inhibitors of mucus hypersecretion are in clinical use but have had limited benefits against COPD. Thus, novel therapies targeting airway mucus hypersecretion should be developed for effective management of muco-obstructive lung disease. Here, we systematically review the mechanisms and pathogenesis of airway mucus hypersecretion, with emphasis on multi-target and multi-link intervention strategies for the elucidation of novel inhibitors of airway mucus hypersecretion.

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