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. 2026 Apr 22;13(1):2662045. doi: 10.1080/20018525.2026.2662045

Narrative review: mucus plugging in chronic obstructive lung diseases and bronchiectasis

Charlotte Schou a,✉, Tuuli Thomander b, Hanna Hisinger-Mölkänen c, Emma Genberg b, Laura Mäkitalo b, Hanna-Riikka Kreivi b, Line Bjerrehave Nielsen a, Witold Mazur b, Paula Kauppi b
PMCID: PMC13103984  PMID: 42038097

ABSTRACT

Background

Mucus plugging, complete intraluminal occlusions, is recurrently found in high-resolution computer tomography images in obstructive lung diseases and is increasingly recognized as clinically meaningful.

Methods

A narrative review on pathophysiology, clinical consequences and treatment of mucus plugging.

Results

In bronchiectasis, mucus hypersecretion and plug formation are associated with infections, such as Pseudomonas aeruginosa and non-tuberculosis mycobacteria and correlated to exacerbations. In chronic obstructive pulmonary disease, mucus plugging is related to greater airflow obstruction, worse health status, higher exacerbation risk, and increased mortality. In asthma, mucus plugging is associated with severe asthma and poorer outcomes. Multiple scoring systems for mucus plugs in chest computed tomography (CT) have been introduced but definitions are heterogenous limiting comparability.

Conclusions

Mucus plugs are measurable markers of disease activity with prognostic relevance across obstructive airway diseases. Clinical adoption is hindered by non‑standardized CT scoring and limited plug‑targeted trials. New treatment options for mucus plugging e.g. biologics in asthma have been found successful, especially dupilumab. Azithromycin as a part of prevention of infections in obstructive lung diseases is effective. Future research is needed to standardize and validate CT-based mucus-plug scoring systems that could be brought into clinical medicine.

KEYWORDS: Sputum, mucus, plug, chronic obstructive airway disease, asthma, bronchiectasis, chronic obstructive pulmonary disease, mucus plugging

Introduction

Mucus plugging, defined as complete intraluminal airway occlusion by inspissated secretions visible on computed tomography (CT), is a common and clinically important finding across obstructive lung diseases [1,2]. In bronchiectasis, chronic obstructive pulmonary disease (COPD), and asthma, plugs are increasingly recognized as markers of disease activity, progression, and prognosis.

In bronchiectasis, mucus plugging contributes significantly to airway damage and disease progression. Typical CT findings include bronchial dilatation, thickened bronchial walls, and tree-in-bud opacities reflecting mucus impaction and active inflammation (Figure 1) [3]. Quantitative imaging tools, such as bronchiectasis CT scoring approaches, have linked higher plug burden to increased infection rates, frequent exacerbations, and greater lung-function impairment [4]. However, multiple scoring approaches exist, and no consensus system has yet been standardized for research or clinical use.

Figure 1.

Diagram of airway structure in COPD showing mucus, cells and pathogens. The image illustrates the airway structure in Chronic Obstructive Pulmonary Disease (COPD). On the left, a cross-sectional view shows the airway lumen surrounded by mucus containing mucins. Goblet cells and glands are present, with plasma proteins and blood vessels nearby. Pathogens and inflammatory cells are depicted within the mucus. On the right, a detailed view shows the airway lumen, mucus gel layer and periciliary layer. Secretory and ciliated cells are visible, with pathogens shown above the mucus layer.

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A cross-sectional view of mucus membrane in a normal bronchus in a large airway and a cross-sectional view of mucous membrane of a small airway and alveolus. Modified from the paper by Fahy JV, Dickey BF (ref Fahy JV, Dickey BF N Engl J Med. 2010).

In COPD, mucus dysfunction is a key abnormality, manifesting as chronic cough and sputum production [5]. CT-identified mucus plugging is frequent and associated with disease severity, reduced health-related quality of life, greater airflow obstruction, increased exacerbation rates, and mortality; higher mucin concentrations identify subgroups at risk of rapid progression, including early COPD [1,5].

In asthma, mucus hypersecretion contributes to persistent inflammation, airway obstruction, and airway remodeling; mucus plugs have been linked to severe asthma, lower lung function, and poorer outcomes [2,6]. These findings highlight plugs as a potential therapeutic target, particularly in T2-high disease.

Although mucus hypersecretion, mucin biology, and inflammatory pathways have been reviewed extensively, the specific clinical significance of mucus plugging itself has received less focused attention, is not routinely assessed in clinical practice and receives limited attention in guidelines. Existing literature is also fragmented across disease-specific fields, making it challenging to determine whether mucus plugging represents a shared clinically meaningful trait across chronic airway diseases or how its relevance differs between disease contexts. In addition, interpretation of the literature is complicated by heterogeneity in CT-definitions and scoring approaches, which limits cross-study comparison and has hindered routine clinical implementation. While several CT scoring systems exist, none are validated for widespread use. Representative CT-based scoring systems are summarized in Table 1. At the same time, emerging evidence suggests that targeted therapies such as biologics in severe asthma or airway-clearance strategies in bronchiectasis may reduce plug burden and improve outcomes [7,8]. This narrative review therefore aims to synthesize current evidence on the clinical impact of mucus plugging in bronchiectasis, COPD and asthma. Specifically, we review the mechanisms contributing to mucus plugging, approaches to its CT-based assessment, and its associations with clinically relevant outcomes including lung function, exacerbations, disease severity, and prognosis. We also discuss therapeutic implications and highlight key knowledge gaps for future research.

Table 1.

Treatment options of mucus plugging in non-cystic bronchiectasis and other airway diseases.

Treatment group Drug or management Dosage Effect
Mucolytics Hyperosmolar solutions (hypertonic saline) or isotonic saline 6% or 7% NaCl inhaled or 0.9% NaCl inhaled To enhance sputum expectoration
  N-Acetylcysteine
Carbocisteine
Erdosteine
Mannitol		   To enhance sputum expectoration and to decrease mucus viscosity
Anti-inflammatory therapy Benralizumab
Dupilumab
Mepolizumab
Omalizumab
Reslizumab
Tetzelumab		   To reduce mucus production and eosinophilic inflammation on bronchial walls
Drugs that reduce mucus production      
Anticholinergics Ipratropiumbromide
Tiotropiumbromide
Aclidiniumbromide
Glycopyrroniumbromide
Umeclidiniumbromide		   To reduce mucus overproduction (indication in COPD or asthma)
Antibiotics Azithromycin 250 mg daily or 500 mg 3 times a week for 3 to 12 months To reduce exacerbations in BE
Airway clearance techniques Cough   To remove bronchial secretions
  Huffing cough   To remove bronchial secretions
  Positive expiratory pressure (PEP)   To remove bronchial secretions
  Flutter device   To loosen and to remove bronchial secretions
  Active cycle of breathing technique   To remove bronchial secretions
  Respiratory muscle training   To remove bronchial secretions
  Chest percussion therapy   To remove bronchial secretions
  High frequency chest wall oscillation vest   To remove bronchial secretions
  Endurance exercise   To remove bronchial secretions
  Rehabilitation   To remove bronchial secretions
  Autogenic drainage   To remove bronchial secretions
  NIV   To open collapsed alveoli and microatelectasis
  HFNC   To preserve airway surface liquid, improve mucociliary function, reduce mucus viscosity
Bronchoscopy     To remove bronchial secretions mechanically
Bronchoalveolar lavage (BAL)     To loosen and to remove bronchial secretions mechanically
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Pathophysiology of mucus plugging

Mucus plugs are visualized on CT as complete intraluminal airway occlusions, most often in medium-to-large bronchi measuring 2–10 mm in diameter and are best detected on thin-slice volumetric reconstructions [9,10]. These radiological findings reflect the underlying pathophysiology: mucin overproduction, impaired clearance, and secretion stasis.

Airway epithelia are lined with ciliated cells and with secretory Club cells and goblet cells (Figure 1). Mucus includes water 97% and other ingredients (3%) such as mucin proteins, lipids, salts and cellular debris. Mucins are glycoproteins and mostly carbohydrates. MUC5AC and MUC5B are glycoproteins found in mucus and are produced by expression of similarly named genes [11,12]. These MUC5AC and MUC5B genes are expressed in human airways, however, cigarette smoke and viruses may further increase expression. In addition, interleukin-4, 9, 13, 17, 23, 25 have been reported to increase expression. Mucins are stored in granules and secreted from these. Secretion can be stimulated by adrenergic, cholinergic, non-adrenergic and non-cholinergic nerve stimulation [9]. Mucus plugging occurs when overproduction or hyperconcentration of mucins is combined with impaired mucociliary clearance [11].

Airway clearance depends on mucociliary transport as well as on airflow dynamics and the cough reflex, which together mobilize mucus from peripheral to central airways [12]. Bronchiectasis is often a consequence of impaired mucociliary function. In primary ciliary dyskinesia (PCD), a well-recognized cause of bronchiectasis, ciliary beating is markedly reduced. Under normal conditions, cilia beat 12–15 times per second to propel the mucus gel layer (mucus and glycoproteins) toward central airways [11]. When this mechanism fails, secretion stasis promotes infection and inflammation. In both bronchiectasis and cystic fibrosis, mucus becomes abnormally thick, and clearance is further compromised by structural airway deformation.

In COPD, airway epithelium and cilia are structurally damaged, leading to impaired clearance of mucus, particularly in central airways. Goblet-cell enlargement and mucin hyperconcentration further contribute to secretion retention [5,12]. These abnormalities create a cycle of obstruction, infection, and inflammation that accelerates disease progression.

Mucus plugging in asthma has been associated with sputum eosinophilia, systemic eosinophilia, increased IL5 and IL13 and further increased expression of MUC5AC and MUC5B genes [2,6]. In addition, when comparing mucus from cases of fatal asthma and chronic asthma, Liegeois et al. showed differences in asthma subtypes and reported paucigranulocytic mucin in fatal asthma and granulocytic mucin in chronic non-fatal asthma [13].

Mucus plugging in bronchiectasis

Bronchiectasis is associated with severe long-term or recurrent infections and other airway diseases such as asthma and chronic obstructive lung disease (COPD), but it may be also idiopathic. Mucus plugging in bronchiectasis displays notable variability across clinical phenotypes [3]. Phenotypes may be differentiated according to different ethiologic systemic diseases, such as Alpha-1-Antitrypsin deficiency or Primary Ciliary Dyskinesia but also according to other clusters of clinical phenotypes. For different traits in bronchiectasis have been suggested e.g. daily sputum production, chronic infection, eosinophilic or T2 high endotype and neutrophilic endotype [14]. These can be used to direct treatment according to background ethiology and clinical phenotype. Anti-inflammatory therapies are used according to eosinophilic and asthma-associated bronchiectasis and mucus plugs. Infectious prevention is directed into recurrent exacerbation, chronic infection and neutrophilic phenotypes (see also later Treatment strategies in mucus plugging).

Bronchiectasis associated with immunodeficiencies like Common Variable Immunodeficiency (CVID) prominently exhibits mucus plugging in approximately 29% of adult cases, typically evident as extensive tree-in-bud patterns [15,16]. Similarly, adult Primary Ciliary Dyskinesia (PCD) frequently demonstrates severe mucus plugging reflecting inherent mucociliary clearance impairment [17]. Another inherited rare disease associated with bronchiectasis is alpha-1-antitrypsin deficiency. In different European non-cystic bronchiectasis cohorts, the prevalence of alpha-1-antitrypsin deficiency has varied from 0.4% to 1% [18]. Cystic fibrosis (CF) is an inherited disease with cystic fibrosis transmembrane conductance regulator (CFTR) protein deficit. It has an impact on chloride channel function in cell membranes and the clinical consequence of the disease is bronchiectasis manifestation in early life. New CFTR modulators show promising results in improving lung function [14].

Systemic inflammatory and autoimmune disorders, including Rheumatoid Arthritis (RA) and Inflammatory Bowel Disease (IBD), are increasingly recognized bronchiectasis phenotypes. Radiologically, mucus plugging is commonly observed in both RA-associated bronchiectasis and bronchiectasis secondary to IBD [19,20]. Similarly, bronchiectasis linked to Sjögren’s disease and aspiration, commonly seen in elderly or neurologically impaired individuals, also frequently present mucus plugging on imaging [3]. However, across these autoimmune and inflammation-driven phenotypes, studies specifically assessing the clinical impact of mucus plugging or phenotype-specific therapeutic interventions remain notably limited, suggesting a relevant area for future research.

Post-infectious bronchiectasis, one of the most common phenotypes, classically demonstrates mucus plugging on CT imaging [21]. Patients with bronchiectasis secondary to nontuberculous mycobacterial (NTM) infection exhibit distinct peripheral mucus plugging patterns, potentially aiding clinical differentiation [22,23]. Dettmer et al. demonstrated that successful NTM treatment led to measurable reductions in bronchiolitis on CT, while mucus plug burden was unchanged [22]. Thus, quantitative links between plug severity and long-term outcomes remain sparse.

Idiopathic bronchiectasis, diagnosed in the absence of identifiable underlying conditions, represents the most prevalent adult phenotype in many study populations. Despite its frequency, no specific studies explicitly compare mucus plugging severity or frequency in idiopathic cases against defined-etiology bronchiectasis groups, constituting a critical, understudied gap [24].

The eosinophilic or T2-high phenotype, frequently observed in bronchiectasis with asthma overlap, correlates with increased mucus plugging (25.9% vs 9.9%; p = 0.017) [25,26]. In addition to asthma, bronchiectasis is a common finding in COPD (Figure 2), however, idiopathic and post-infective phenotypes dominate in Europe [26]. Traction bronchiectasis can be found also in smoking related interstitial disease and in association with pulmonary fibrosis [27].

Figure 2.

Illustration of large and small airways showing mucus gel, smooth muscle, bronchiole, alveolus and capillary. On the left, the large airway is shown with a mucus gel layer and a periciliary layer. It includes smooth muscle, submucosal gland and cartilage. On the right, the small airway is divided into bronchiole and alveolus sections. The bronchiole features smooth muscle, while the alveolus includes Type 1 and Type 2 pneumocytes, surfactant and a capillary. The capillary is depicted with red blood cells inside. The image highlights the anatomical differences between the large and small airways, emphasizing the presence of various cellular and structural components.

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A cross-sectional view of bronchiectatic bronchus in COPD associated bronchiectasis and a cross-sectional view of mucous membrane in a respective situation. Modified from the paper by Fahy JV, Dickey BF (ref Fahy JV, Dickey BF N Engl J Med. 2010).

Lastly, Yellow Nail Syndrome (YNS) which often involves lymphatic dysfunction, distinctively demonstrates prominent mucus plugging compared to idiopathic bronchiectasis. Its characteristic predominant bilateral lower lobe plugging highlights how specific, extrapulmonary mechanisms significantly influence airway mucus dynamics [28]. Collectively, the diversity among bronchiectasis phenotypes, particularly exemplified by both NTM, eosinophilic and YNS, suggests a crucial clinical message: effective management of mucus plugging in bronchiectasis should be phenotype-specific, addressing the distinct underlying cause of mucus plugging. Additionally, across phenotypes, comprehensive quantitative studies evaluating mucus plugging severity and targeted clinical trials are needed to develop tailored therapeutic strategies.

Mucus plugging in COPD

COPD is characterized by progressive airflow limitation and recurrent exacerbations, often linked to chronic bronchitis and emphysema. Mucus plugging is increasingly recognized in COPD as a structural marker of disease activity, present in 25–78% of patients during stable disease and up to 78% during acute exacerbations [29–32]. Notably, plugs are also detected in patients without typical sputum symptoms [33].

The presence of mucus plugs has also been associated with increased airway wall thickening as demonstrated in Tran et al., and furthermore, plugs located in medium-to-large airways may contribute to progressive airflow obstruction beyond that attributable to emphysema alone [30,34] (Figure 2).

Mechanistically, plugs may obstruct airflow and impair gas exchange by creating regions of ventilation-perfusion mismatch contributing to localized hypoxia. These effects are exacerbated by impaired mucociliary clearance, allowing mucus-filled segments to serve as reservoirs for chronic bacterial colonization, which sustains neutrophilic inflammation and may increase both the frequency and severity of exacerbations as well as poorer prognosis [35,36].

Importantly, mucus plugs in COPD appear more closely linked to neutrophilic inflammation and bacterial colonization than to eosinophilic phenotypes [36,37]. This is consistent with the Korean study where plug-related exacerbation risk was particularly elevated in non-eosinophilic phenotypes, which are associated with worse clinical outcomes [38–41]. In contrast to asthma, where plugs are more often eosinophilic, the COPD phenotype is generally characterized by type 1 inflammation. However, recently also eosinophilic phenotype in COPD has been introduced and biologics as a therapeutic option in a such case [42].

Mucus plugging in asthma

Mucus plugging has previously been associated with acute and fatal asthma, but recent studies have increased the understanding of the role of mucus plugs in chronic asthma [13]. Mucus plugs can be found both in those with symptoms of overproduction of phlegm but also in asymptomatic (no symptoms of phlegm production) patients [2]. Not all asthma patients develop persistent mucus plugging, but CT-based studies report prevalence rates of 53–58% across mixed-severity populations and up to 77% in severe biologic-naïve patients initiating biologic therapy [2,43,44]. In a CT-based longitudinal study of 146 asthma patients, plugs were not only present in 66% of those with severe asthma but persisted for over 3 years, with progression to higher plug scores in patients unresponsive to bronchodilators and inhaled corticosteroids [2].

Plug formation in asthma is heterogeneous, reflecting overlap between type 2 (T2) and non-T2 inflammation. Specific IgE antibodies and sputum eosinophils were not significantly associated with mucus plug scores in asthma patients in a recent study whereas serum total IgE and FeNO correlated with mucus plug score [38]. Peripheral eosinophil count has been reported to correlate to mucus plug scores in non-smoking patients with eosinophilic or non-eosinophilic asthma but not to either of these in smokers [45]. Higher FeNO has been associated with higher rate of mucus plugging in patients with asthma despite whether they are former smokers or nonsmokers [46].

In patients with difficult-to-treat asthma and Aspergillus fumigatus sensitization, mucus plugs are found significantly more frequently than in non-sensitized patients [47]. Furthermore, allergic bronchopulmonary aspergillosis (ABPA) may also lead into mucus plugging. In this disease, characterized by sensitization and colonization to aspergillus, glucocorticoids have been used in addition to asthma medication as therapy and then antifungal treatments and lately also biologicals [48].

The mechanistic link between interleukines and mucin helps explain why mucus plugs are consistently associated with more severe asthma, including reduced lung function, higher exacerbation frequency, and elevated T2 biomarkers [2]. It is therefore not surprising that plugs are increasingly recognized as a hallmark of severe, T2-high disease.

Clinical impact of mucus plugging in bronchiectasis, COPD and asthma

Mucus plugging is a key determinant of clinical outcomes and disease severity in bronchiectasis. A high plug burden on CT, particularly when >9 bronchopulmonary segments are involved, correlates with higher severity scores (FACED, modified Reiff), impaired lung function, and elevated markers of airway inflammation such as sputum myeloperoxidase [4,49]. In this same study, baseline mucus plug presence was independently associated with significantly increased risks of moderate-to-severe exacerbations (HR 1.50), severe exacerbations (HR 2.11), and specifically non-eosinophilic exacerbations (HR 1.55; all p < 0.05). Patients also experienced accelerated annual FEV1 decline (β = −62 mL/year; p = 0.035), underscoring mucus plugging as a predictor of progressive airway deterioration [49]. Mucus plugging predict increased systemic inflammation and greater symptom burden, including persistent cough, sputum production, dyspnea, and fatigue, airway obstruction, higher rates of Pseudomonas colonization collectively leading to diminished quality of life, impaired functional status over time and increased mortality risk [4,24].

Quantitatively assessed mucus plugs on CT also correlate with advanced disease markers such as obstructive and restrictive lung defects, decreased gas diffusion capacity, and potentially increased mortality, emphasizing their significance as markers of severe disease [30]. This highlights a need for prospective longitudinal studies specifically evaluating quantitative mucus-plug scores against long-term clinical outcomes, particularly symptom trajectories, functional decline, and mortality, to clearly establish mucus plugging as a clinically meaningful biomarker.

The presence of mucus plugs is associated with airflow obstruction independent of emphysema, increased symptoms, poorer quality of life and higher mortality [31,40,43,50]. Longitudinal imaging has shown that plugs persist in a majority of patients over 1–5 years, reinforcing their potential role in disease progression [1,34].

These structural and inflammatory sequelae may explain the observed association between mucus plug burden and exacerbation frequency in several large-scale cohort studies. Patients with plugs in one or more bronchopulmonary segments exhibit higher rates of moderate-to-severe exacerbations, with highest risk when plugs affect ≥3 segments [1,35].

In a histopathological study, Hogg et al. found that occlusion of small airways with mucus was associated with early death in patients undergoing lung volume reduction surgery [50]. Similarly, an observational study of 4,363 patients with COPD found that mucus plugs occluding medium- to large-sized airways (2–10 mm in diameter) were significantly associated with higher mortality risk: adjusted hazard ratios were 1.15 and 1.24 for 1–2 and 3 affected segments, respectively [10]. These findings support the hypothesis that mucus plugs are not merely markers of disease burden but may actively contribute to COPD progression. By impairing ventilation, perpetuating inflammation, and fostering colonization, mucus plugs represent a mechanistic link to both exacerbation risk and increased mortality. A prospective Japanese cohort study similarly found that high mucus scores, rather than airway count or emphysema extent, were independently associated with 10-year mortality [32].

Mucus plug scores correlate inversely with lung function in asthma. Patients with plugs have significantly lower FEV1%, PEF and FVC% compared with those without [46]. One study contradicted the association between FVC% and mucus plugs in asthma patients despite the smoking status or Th2 inflammation [46]. Patients with eosinophilic asthma tend to have higher mucus plugs scores and lower FEV1% when compared to those with non-eosinophilic asthma, and the results remain similar in patients with severe asthma [46]. Mucus plugs in proximal airways have greater effect on lung volume, whereas mucus plugs located in peripheral airways are associated with local air trapping, harder to recognize with standard spirometry [51].

Moreover, eosinophil peroxidase excreted by airway eosinophils stiffen the hydrogels in mucus and contribute to plug formation [52]. Hence type 2 inflammatory mechanisms can alter mucus composition leading to sticky mucus that is hard to expectorate and functions as a platform for pathogen growth and can further augment exacerbations [53]. Currently, CT imaging is considered as the golden standard for evaluating mucus plugs. Mucus plug score, a clinical tool developed by Dunican et al. with a range from 0 to 20 (the number of pulmonary segments affected by mucus plugs) is an attempt to utilize current understanding in the treatment planning and follow up [45]. Asthma Control Test (ACT) result has been reported to be significantly lower in those with persistent mucus plugs and change in airway mucus plug score from baseline to 3-year control was negatively correlated with ACT [54]. The international guideline for severe asthma, GINA, recommends considering a CT scan mainly for differential diagnostics [55]. Studies evaluating the predicting role of a CT scan have been lacking. However, the routine evaluation of mucus plugs remains limited in clinical practice due to lack of protocols and availability of advanced imaging resources.

In summary, mucus in the airways induces chronic airway inflammation and may induce even epithelial necrosis, retention of inhaled allergens and microbes [56]. The clinical impact of mucus plugging in bronchiectasis, COPD and asthma is to add the severity of the disease; poorer quality of life, reduced lung function, increased exacerbation risk and mortality.

Treatment strategies for mucus plugging

Therapeutically, effective mucus management is fundamental. Hypertonic saline is commonly employed to improve mucociliary clearance, facilitating sputum expectoration, although adult bronchiectasis trials have yielded variable improvements in symptoms and lung function [55,57]. Mucolytics, including mannitol, N-acetylcysteine, and carbocisteine, aim to modify mucus characteristics to enhance clearance (Table 2). These agents show variable clinical efficacy, with some studies reporting reduced exacerbation frequency and improved sputum clearance [55,58]. Additionally, erdosteine, a thiol-based mucolytic approved in certain regions for bronchiectasis, has demonstrated benefits in mucus viscosity and possibly exacerbation duration [58]. In a recent study, carbocisteine did not show any benefit for exacerbations in bronchiectasis during 1 year of treatment [59].

Table 2.

Different cytokine specific anti-inflammatory medication options in obstructive lung diseases.

  Drug Effect
IL4/IL13 antibody Dupilumab Mucus hypersecretion ↓
Bronchial smooth muscle tone↓
IL5R antibody Benralizumab Mucus hypersecretion ↓
Reduction in eosinophilic inflammation
IL5 antibody Mepolizumab Reduction in eosinophilic inflammation
  Reslizumab Reduction in eosinophilic inflammation
IgE antibody Omalizumab Reduction in IgE dependent inflammation
TSLP antibody Tezelumab Mucus hypersecretion ↓
Bronchial smooth muscle tone↓
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Despite the mechanism, non-pharmacological therapies, like hydration therapy, may enhance mucus clearance. Hypertonic saline has been used in bronchiectasis, as it reduces mucus viscosity, improving airway clearance. Lower concentrations are not as effective. However, lately it was not shown to reduce number of exacerbations in bronchiectasis during one year follow-up [59].

Mechanical airway clearance therapies (e.g. chest physiotherapy, oscillatory devices) remain cornerstone treatments, particularly validated in mucociliary dysfunction phenotypes like Primary Ciliary Dyskinesia (PCD), demonstrating slower disease progression and fewer infections [17]. Airway clearance therapies have been suggested to reduce ventilation-perfusion mismatch and to reduce breathlessness [60]. Nonetheless, randomized controlled trials explicitly targeting mucus plugging via CT quantification are notably lacking. Further, treatment adherence to both pharmacologic treatment and airway clearance therapies and its impact on the mucus plugs should be studied.

Long-term antibiotic therapies with macrolides have anti-inflammatory effects in addition to antimicrobial ones in asthma. A reduction in goblet cell metaplasia and mucin expression lead to decreased mucus secretion. However, we lack placebo-controlled studies of macrolides for mucus plugging in asthma. Furthermore, long-term antibiotic use may lead to antibiotic resistance and therefore is controversial, especially as we nowadays have other options [61–63].

In a case series of unilateral pulmonary collapse due to allergic bronchopulmonary aspergillosis (ABPA), flexible bronchoscopy was performed to remove mucus plugs from the obstructed airways but was ineffective in 4/5 cases. A rigid bronchoscopy and the use of a cryobiopsy probe may be helpful to rapidly remove large plugs [64].

Treatment with anti-inflammatory medication

Biological therapies have shown promising results in severe asthma with mucus plugging and mucus plugging has been proposed as a prognostic indicator for biologic treatment response in severe asthma [65]. Several studies have reported efficacy in mucus plugs with biological treatment. Benralizumab has been reported to have improved asthma control and ventilation already after a single dose in patients with more than five mucus plugs, and the result persisted 2.5 years later [51]. A placebo-controlled study reported similar results with dupilumab as mucus plugging was reduced in a relatively short time period (16 weeks) although residual mucus plugs persisted in 46% of patients [7]. Similarly, in a double-blind, placebo-controlled trial on tezepelumab, mucus plugs were reduced in the tezepelumab group [66].

In the study of Castro et al., dupilumab 300 mg every other week decreased mucus plug scores compared to the baseline and compared to the placebo [7] (Table 3). In addition, dupilumab reduced mucus volume. The mucus plug score diminishing was detectable in CT scans. Simultaneously with the reduction in mucus plug scores there was a reduction in airway resistance (R5–R20) [6]. This was considered a consequence of improved airflow in the small airways.

Table 3.

Different cytokine specific anti-inflammatory medication options in obstructive lung diseases.

  Drug Effect
IL4/IL13 antibody Dupilumab Mucus hypersecretion ↓
Bronchial smooth muscle tone↓
IL5R antibody Benralizumab Mucus hypersecretion ↓
Reduction in eosinophilic inflammation
IL5 antibody Mepolizumab Reduction in eosinophilic inflammation
  Reslizumab Reduction in eosinophilic inflammation
IgE antibody Omalizumab Reduction in IgE dependent inflammation
TSLP antibody Tezelumab Mucus hypersecretion ↓
Bronchial smooth muscle tone↓
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IL-5 antibodies (mepolizumab, reslizumab) and IL-5-receptor antibody (benralizumab) have been effective in reducing mucus plugs in asthma. In a German study, baseline mucus plug score was correlated with greater change in FEV1 and in Asthma Control Test during any biological asthma therapy [44]. In this study, FEV1(%), FVC(%), PEF(%), and diffusion capacity for carbon monoxide (%) increased during biological therapy. In addition, residual volume decreased.

Case reports have been published of treatment efficacy also with mepolizumab [67]. Also, a case report with successful treatment with a rapid improvement in bronchial mucus plugs by benralizumab has been described [68]. In addition, dupilumab has led to successful improvement of mucus plugs in a patient with ABPA and asthma and limited previous response to mepolizumab [52].

Mucus plugs and non-invasive ventilation (NIV) or high-flow nasal therapy (HFNT) treatment

Both NIV and HFNT treatment are used in COPD patients with severe exacerbation and the latter also in any severe acute pulmonary infection when necessary. While there is no direct evidence that NIV directly treats mucus plugs, it helps to open collapsed alveoli and microatelectasis [69,70] which might assist in clearing secretions and reducing the impact of mucus plugs. The positive pressure provided by NIV decreases the effort required for breathing, alleviating the strain on inspiratory muscles [70]. Improvement in lung function [71] may indirectly help in the management of mucus plugs.

In HFNT treatment, heated, fully humidified gas preserves airway surface liquid, improves mucociliary function, reduces mucus viscosity, and aids secretion clearance [72]. In patients with bronchiectasis, long-term HFNT treatment has been associated with significant improvements in CT-assessed mucus scores [8]. For stable COPD with frequent exacerbations and/or hypercapnia, home HFNT at night reduces exacerbations and may help CO2 retention in selected patients [73]. To our knowledge, there are no direct trials on obstructive disease patients focused specifically on mucus plugs yet. However, evidence from related airway diseases indicates that HFNT improves mucociliary clearance and facilitates secretion mobilization [72].

Non-invasive ventilation was shown to be a good alternative to PEP in chest physiotherapy for patients with cystic fibrosis who are severely ill [74]. The respective results could be expected in non-cystic fibrosis bronchiectasis but have not been studied in detail.

Future perspectives

Future research should prioritize developing standardized CT-based mucus-plug scoring systems validated against clinical outcomes, conducting phenotype-specific intervention trials explicitly targeting mucus plugging, and performing longitudinal studies assessing mucus plugging as a biomarker for disease progression. Automated plug quantification methods should be developed for CT-scan imaging, to be used to identify patients with greater risk of worse symptoms, poorer prognosis and shorter life expectancy. Mucus plugs might be considered as a treatable trait in obstructive lung diseases and thus relevance in treatment planning. Addressing these priorities will substantially refine personalized treatment strategies, ultimately enhancing patient-centered outcomes and clinical management.

Acknowledgments

Thank you for Soile Lätti for the help with the Figures.

We used ChatGPT (OpenAI; model GPT-5 Pro) to aid literature discovery and language improvement; all content was verified and edited by the authors, who take full responsibility for the manuscript.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Abbreviations

ABPA

Allergic Bronchopulmonary Aspergillosis

ACT

Asthma Control Test

ACQ

Asthma Control Questionnaire

BEST-CT

Bronchiectasis Scoring Technique for computer tomography

BSI

Bronchiectasis Severity Index

CF

Cystic Fibrosis

COPD

Chronic Obstructive Pulmonary Disease

CVID

Common Variable Immunodeficiency

FACED

Score to estimate bronchiectasis severity (FEV1, age, chronic colonization of Pseudomonas Aeruginosa, extent of disease radiologically and dyspnea)

FeNO

Fractional exhaled nitric oxide

FEV1

Forced expiratory volume in one second

FVC

Forced vital capacity

HFNT

High flow nasal therapy

HRCT

High Resolution Computed Tomography

IBD

Inflammatory Bowel Disease

ICS

Inhaled Corticosteroids

NIV

Non-invasive ventilation

NTM

Nontuberculous mycobacterial infection

OCS

Oral Corticosteroids

PEF

Peak Expiratory Flow

PCD

Primary Ciliary Dyskinesia

RA

Rheumatoid Arthritis

SpO2

Peripheral oxygen saturation

T2

T helper (2) type lymphocytes

YNS

Yellow Nail Syndrome

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