What Is Asthmatic Airway Remodeling?

Asthma is characterized by changes in the structure and composition of the airway walls, collectively known as airway remodeling. These changes include increased numbers of mucus-secreting epithelial cells, thickening of the subepithelial collagen layer, and increases in vascularity and smooth muscle mass around the airways. Airway remodeling is a complex clinical feature of asthma that involves long-term disruption and modification of airway architecture. It is associated with narrowing of the airway lumen and an increased thickness of the airway wall, although not usually to the extent seen in asthma.

Airway remodeling is characterized by goblet cell hyperplasia, subepithelial fibrosis, and hyperplasia and hypertrophy of airway smooth muscle. The increase in the ASM mass contributes to bronchial obstruction, loss of lung function, and greater susceptibility to external triggers. This review explores three integrated and dynamic processes in airway remodeling: initiation by epithelial cells; amplification by immune cells; and fibroblast activation.

In asthma, airway remodeling is characterized by subepithelial fibrosis, increased smooth muscle mass, gland enlargement, neovascularization, and epithelial alterations. These structural changes are a key feature in the pathogenesis of asthma, leading to thickened airway walls and narrowing of the airway. The phenomenon is complex and requires reliable quantitative approaches to assess and support the notion that airway remodeling is a collective term that encompasses alterations in structural cells and tissues.

Is airway remodeling permanent?

Airway remodelling is a process triggered by asthma that results in thickened airway walls and narrowing of the airway. This process can lead to irreversible changes to the airway structure, potentially causing blockages and long-term loss of lung function. The longer asthma symptoms are uncontrolled or untreated, the more likely airway remodelling will occur. Asthma triggers inflammation in the lungs, and the body tries to repair itself by thickening the membrane below the cells.

This process results in more blood vessels and an increased layer of smooth muscle surrounding the airway, altering the airway’s structure and function, potentially leading to bronchoconstriction and an irreversible decrease in lung function.

How do you tell if you have airway remodeling?

Airway remodeling is a condition where airway membranes thicken, larger muscles and mucus glands grow, and scar tissue under the airway lining grows, narrowing the airways and causing asthma symptoms. However, the exact definition of this condition and its impact on asthma patients remain unclear. Researchers are exploring the link between asthma severity and airway remodeling, as well as if remodeling is responsible for the exaggerated response to asthma triggers and lower lung function. Further research is needed to understand the early stages of remodeling, its development over time, and if treatment can prevent or reduce symptoms.

How do you prevent airway remodelling in asthma?

To prevent airway remodelling, asthma symptoms should be controlled through a treatment plan and medication that reduces airway inflammation. The less asthma symptoms experienced, the less airway remodelling will occur. Some remodelled airways can return to normal structure when proper treatment is followed. People with asthma already have trouble breathing, so controlling their asthma is crucial. Diana Pham’s research on airway remodeling mechanisms can provide further insight.

How do I know if I have airway remodeling?

Airway remodeling is a condition where airway membranes thicken, larger muscles and mucus glands grow, and scar tissue under the airway lining grows, narrowing the airways and causing asthma symptoms. However, the exact definition of this condition and its impact on asthma patients remain unclear. Researchers are exploring the link between asthma severity and airway remodeling, as well as if remodeling is responsible for the exaggerated response to asthma triggers and lower lung function. Further research is needed to understand the early stages of remodeling, its development over time, and if treatment can prevent or reduce symptoms.

Can you reverse airway remodelling?

Airway remodeling in asthma is a common issue that is difficult to reverse once it occurs. Currently, there are no drugs or interventions available that can completely reverse airway remodeling in asthma. Reversing airway remodeling can not only relieve asthma symptoms but also prevent disease progression and improve prognosis. Glucocorticoid therapy, which is the first-line treatment for airway inflammation in asthma, has been shown to inhibit airway remodeling by inhibiting the metaplasia of goblet cells, the hypertrophy and phenotypic transition of ASM cells, the proliferation of lung fibroblasts, the release of inflammatory mediators, and the thickening of the subepithelial RBM. However, up to 1/3 of asthma patients are clinically insensitive to glucocorticoid therapy, which may play an important role in airway remodeling.

Anti-IgE therapy, which binds specifically to circulating IgE molecules, has been introduced into asthma treatment. Omalizumab, a humanized, monoclonal anti-IgE antibody, has been well documented in numerous clinical trials in patients with moderate to severe persistent allergic asthma. Studies have shown that omalizumab interrupts the allergic cascade by preventing IgE from binding to mast cells, basophils, and antigen-presenting cells, alleviating inflammatory cell infiltration, decreasing bronchial mucosal fibronectin deposition and RBM thickness, and even acting directly on IgE-bound ASM cells, helping to reverse airway remodeling.

Pregnancy-associated plasma protein-A and galectin-3 may be useful biomarkers for predicting airway remodeling in patients with severe asthma treated with omalizumab. However, it has been suggested that omalizumab may have a limited effect on airway remodeling, necessitating larger multicenter clinical trials.

What are the steps that lead to airway remodeling?

Multiple pathogenic factors trigger structural alterations in the normal airway wall, including epithelial cell shedding, goblet cell hyperplasia, basement membrane thickening, smooth muscle cell hyperplasia and hypertrophy, and bronchial angiogenesis. These changes are triggered by various factors, including bronchial angiogenesis. ScienceDirect uses cookies and all rights are reserved, including those for text and data mining, AI training, and similar technologies. Creative Commons licensing terms apply for open access content.

What is airway inflammation and remodeling in asthma?

Chronic allergic airway inflammation induces airway remodeling, which is resistant to asthma therapy. Early intervention with inhaled corticosteroid should be considered to prevent the progression of this remodeling. This is because cytokines and mediators produced in chronic allergic airway inflammation are involved. Copyright © 2024 Elsevier B. V., its licensors, and contributors. All rights reserved, including text and data mining, AI training, and similar technologies.

What are the mechanisms of airway remodeling in asthma?

Asthma is a common condition affecting 30-50% of individuals with fixed airway obstruction, with severe or difficult-to-treat adult asthmatics having 55-60 fixed airway obstructions. Airway remodeling may explain persistent airflow obstruction in some asthmatic patients, attributed to factors such as goblet cell hyperplasia, decreased epithelial cell and cartilage integrity, subepithelial collagen deposition, increased airway smooth muscle mass, and angiogenesis of the airways.

This is present in asthmatics with mild disease but tends to worsen with increasing disease severity. The onset of airway remodeling has been identified in pre-school children as young as 1-year-old and persists through adulthood. However, adult asthma patients with minimal airway remodeling similar to healthy controls have also been identified, and adult mild asthmatics acutely increase parameters of airway remodeling with exposure to asthma triggers.

Personalized medicine in asthma care has benefitted from the recognition that “asthma” refers to an umbrella term encompassing a range of clinical presentations. The goal of phenotyping asthmatics is to link clinical phenotype to molecular mechanisms, defining an “endotype” that would predict response to therapy. Four subgroups of adult asthmatics were identified: eosinophilic asthma, neutrophilic asthma, mixed granulocytic asthma with both sputum eosinophils and neutrophils, and paucigranulocytic asthma with neither. The distribution of asthma favors eosinophilic (40-50) and paucigranulocytic (30-50) airway inflammation, with only 10-20 of patients manifesting neutrophilic asthma.

What happens in airway remodelling?

Airway remodelling refers to structural changes in both large and small airways, which are linked to various diseases, including asthma. These changes include subepithelial fibrosis, increased smooth muscle mass, gland enlargement, neovascularization, and epithelial alterations. Research has shown that reticular basement membrane thickness is linked to airway wall remodeling in asthma. Additionally, subepithelial fibrosis is observed in the bronchi of asthmatics. These findings highlight the importance of understanding the role of airway remodeling in asthma management.

What is tissue remodeling in asthma?

Asthma is a chronic inflammatory disease of the airways, resulting in structural alterations known as airway remodeling. Despite extensive research, the precise mechanisms underlying this process remain largely unknown.

What causes airway remodelling?

Asthma is a condition characterized by airway structural changes such as subepithelial fibrosis, increased smooth muscle mass, gland enlargement, neovascularization, and epithelial alterations. These changes are often linked to an underlying chronic inflammatory process. Airway remodeling is often attributed to this inflammatory process. Studies have shown that subepithelial fibrosis is present in the bronchi of asthmatics. The relationship between reticular basement membrane thickness and airway wall remodeling in asthma is controversial.