Unraveling the obesity–asthma link: A new horizon with glucagon-like peptide-1 receptor agonists in a complex intersection of metabolism and airway disease

Abstract

The global prevalence of obesity and asthma has escalated in parallel over recent decades, presenting an intertwined public health crisis. Obesity not only increases the risk of asthma development but also complicates its clinical course by altering respiratory mechanics, immune responses, and treatment responsiveness. Obesity-associated asthma is often more severe, less responsive to corticosteroids, and accompanied by systemic comorbidities such as insulin resistance and metabolic syndrome. Recently, glucagon-like peptide-1 receptor agonists, initially approved for diabetes and obesity, have shown potential in improving asthma outcomes. Preclinical data and early clinical studies suggest that glucagon-like peptide-1 receptor agonists exhibit anti-inflammatory and immunomodulatory effects independent of their metabolic benefits, in addition to a possible role in improving the respiratory function of the large and small airways impaired in obese patients with asthma. This narrative review examines the pathophysiological interplay between obesity and asthma, evaluates the current evidence supporting the use of glucagon-like peptide-1 receptor agonists in this context, and highlights the emerging paradigm of treating asthma as a systemic, multifactorial disease. Targeting metabolic dysfunction with glucagon-like peptide-1 receptor agonists may represent a potential transformative approach for patients with obesity and difficult-to-treat asthma.

Keywords

Obesity asthma glucagon-like peptide-1 receptor agonists inflammation respiratory function airway disease semaglutide

Introduction

Obesity and asthma are two of the most prevalent chronic diseases globally. Each affects hundreds of millions of individuals and contributes significantly to morbidity, healthcare utilization, and impaired quality of life. Although they were once considered distinct conditions, growing research has revealed notable interactions between excess adiposity and airway disease. In particular, obesity is now recognized as both a risk factor for asthma onset and a modifier of asthma severity and treatment response.^1,2

The coexistence of obesity and asthma represents a challenging clinical phenotype, characterized by poor asthma control, increased risk of exacerbations, and reduced responsiveness to standard therapies, particularly inhaled corticosteroids (ICS). Moreover, individuals with obesity often experience overlapping symptoms from comorbidities, such as obstructive sleep apnea (OSA), gastroesophageal reflux disease (GERD), and metabolic syndrome, complicating diagnosis and management.

In this complex clinical landscape, there is an urgent need for therapeutic strategies that address both airway inflammation and systemic metabolic dysfunction. One such class of agents—glucagon-like peptide-1 receptor agonists (GLP-1 RAs)—has emerged as a potentially powerful tool, which was initially developed for glycemic control in type 2 diabetes mellitus (T2DM) and subsequently approved for weight loss. GLP-1 RAs may also benefit patients with obesity-associated asthma.^3,4

This narrative review provides an in-depth overview of the pathophysiological links between obesity and asthma, highlights the limitations of current management strategies, and examines the scientific rationale and emerging evidence supporting the use of GLP-1 RAs as a novel treatment option in this setting.

Methods

Data sources and study selection

We conducted a review of literature to identify articles on obesity and asthma and GLP-1 RA treatment as well as relevant clinical trials and reviews that were published in English from the inception of the databases until September 2025. The biomedical bibliographic databases reviewed included MEDLINE (PubMed), Scopus, Web of Science, Google Scholar, and Embase. The search terms used were “asthma,” “obesity,” “GLP-1 RA,” “lung function,” “outcomes,” “biologics,” clinical studies,” and “exacerbations.”

This narrative review was conducted in accordance with the Scale for the Assessment of Narrative Review Articles (SANRA).⁵

The obesity–asthma link: epidemiology and phenotypic complexity

Numerous epidemiological studies have demonstrated that obesity increases the risk of developing asthma. A meta-analysis of prospective cohort studies reported that individuals with obesity (body mass index (BMI) ≥30 kg/m²) had a 1.5-fold higher risk of developing asthma compared with those with normal weight.⁶ This association is particularly pronounced in adult-onset asthma, wherein obesity often precedes symptom onset, suggesting a causal link.

Asthma in individuals with obesity is often more severe and difficult to control. This phenotype is characterized by a higher symptom burden despite preserved spirometry, reduced responsiveness to ICS, increased frequency of exacerbations, poorer quality-of-life scores, and greater healthcare utilization.⁷ Notably, not all individuals with obesity and asthma present the same way. At least two distinct sub-phenotypes have been described: (a) Early-onset asthma with obesity. Typically allergic (T helper 2 (Th2)-high), eosinophilic, and responsive to ICS, but worsened by obesity and (b) Late-onset obesity-related asthma. Often noneosinophilic, less allergic, and neutrophilic or pauci-granulocytic, with a blunted response to corticosteroids.⁸

Understanding these endotypes is essential for developing potential targeted therapies.

Pathophysiology of obesity-associated asthma

The mechanisms linking obesity and asthma are multifactorial and include the following:

Altered lung mechanics and small airway dysfunction (SAD)

Obesity reduces lung volumes, such as functional residual capacity (FRC) and expiratory reserve volume (ERV), leading to decreased airway diameter and increased airway resistance. This mechanical effect contributes to dyspnea and increased work of breathing, which may be misinterpreted as worsening asthma.⁹ Another relevant aspect in obese patients with asthma is the presence of significant peripheral airway dysfunction detected by oscillometry, disproportionate to the airway abnormalities identified by spirometry.¹⁰ SAD represents a clinically significant feature not easily assessed by spirometry and is an independent risk factor for poor asthma control, characterizing SAD as a “treatable lung trait” in obese individuals with asthma. Oscillometry may significantly improve the quality of care in this subgroup of patients.¹¹ Recent studies support the hypothesis that obesity predisposes individuals to peripheral airway reactivity.¹² Two distinct groups of asthma have been identified based on respiratory system impedance: (a) Low-responsiveness group: Baseline AX 11.8 (interquartile range (IQR), 9.9–23.4 cm H₂O/L), with more concordant bronchoconstriction in the central and peripheral airways and (b) High-responsiveness group:. Baseline AX 46.7 (IQR, 23.2–53.5 cm H₂O/L), with discordant bronchoconstriction responses between central and peripheral airways. This group consisted exclusively of women and was associated with GERD, increased chest tightness, and dyspnea compared with the low-responsiveness group.

Furthermore, recent evidence indicates that adipose tissue can accumulate within the airway walls themselves, causing mechanical obstruction and airway narrowing independent of lung compression.^13–14

Systemic and airway inflammation

Obesity is a state of chronic low-grade inflammation, characterized by elevated circulating levels of pro-inflammatory cytokines, including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and leptin, and decreased levels of anti-inflammatory adipokines such as adiponectin.¹⁵ Previous studies have also shown that individuals with asthma and obesity exhibit significantly greater expression of neutrophils, IL-5, IL1-7A, and IL-25 messenger ribonucleic acid (mRNA) in sputum compared with individuals with asthma alone.¹⁶ These mediators can influence airway inflammation and remodeling, contributing to asthma pathogenesis (Table 1). In this regard, we look forward to results from a prospective trial, using the neutrophil modulator azithromycin, on the primary outcome of exacerbation frequency in patients with coexisting asthma and obesity.¹⁷

Table 1.

Key pathophysiological mechanisms linking obesity and asthma.

Pathophysiological domain	Mechanism	Clinical impact
Lung mechanics	Decreased FRC and ERV; increased Rrs_5-20 and AX	Airway closure, dyspnea, reduced lung compliance
Adipose tissue inflammation	Increased leptin, IL-6, TNF-α; decreased adiponectin; increased IL-5, IL-17A, and IL25 in sputum	Airway inflammation, systemic immune dysregulation
Immune profile shift	From Th2 (eosinophilic) to Th1/Th17 (neutrophilic) inflammation	Steroid resistance, poor response to biologics
Insulin resistance	Hyperinsulinemia-induced ASM proliferation	Airway remodeling, fixed obstruction
Comorbidities	OSA, GERD, depression, dyslipidemia, physical inactivity	Exacerbation of asthma symptoms, reduced quality of life
Mechanical ventilation effects	Abdominal fat compressing diaphragm, altered chest wall mechanics	Increased work of breathing, sensation of airflow limitation

FRC: functional residual capacity; ERV: expiratory reserve volume; Rrs_5-20: difference in respiratory resistance between 5 Hz and 20 Hz; AX: reactance area; IL: interleukin; TNF-α: tumor necrosis factor-alpha; Th: T helper; ASM: airway smooth muscle; OSA: obstructive sleep apnea; GERD: gastroesophageal reflux disease.

Insulin resistance and metabolic syndrome

Insulin resistance, a hallmark of obesity and T2DM, is independently associated with reduced lung function and an increased risk of asthma. Hyperinsulinemia has been shown to enhance airway smooth muscle proliferation and fibrosis, contributing to airway remodeling.¹⁸

Altered immune responses

Individuals with obesity may exhibit a shift from Th2 (eosinophilic) to Th1 or Th17 (neutrophilic) inflammation, reducing the efficacy of corticosteroids. This shift contributes to the development of non-T2 asthma, which is less responsive to current biologic therapies and ICS.¹⁹

Comorbid conditions

OSA, GERD, depression, and physical inactivity are more prevalent in obesity and can exacerbate asthma symptoms or mask therapeutic response.

Limitations of current treatment strategies

Current asthma management guidelines are primarily based on clinical trials conducted in non-obese populations. In patients with obesity, the response to ICS is often attenuated, particularly in those with non-T2 inflammation.²⁰ Even high-dose ICS/long-acting beta-2 agonist (LABA) combinations may provide limited benefit, sometimes necessitating oral corticosteroids (OCS) or additional biologic therapies in severe cases.

Although biologics targeting T2 pathways (e.g. anti-immunoglobulin E (anti-IgE), anti-IL-5, and anti-IL-4/13) can be effective, their response may be less predictable in obese patients, who often exhibit non-T2, pauci-granulocytic inflammation. Similarly, the use of OCS carries a significant risk of exacerbating underlying metabolic comorbidities common in this population, including insulin resistance and weight gain.^21,22

Lifestyle modification and weight loss are recommended and have been associated with improvements in quality of life. However, they have not consistently been shown to improve symptom control or reduce exacerbation frequency compared with usual care, and sustaining these interventions can be challenging.²³ Although bariatric surgery can lead to substantial and sustained improvements in asthma control, exacerbation rates, and medication requirements, it is an invasive procedure reserved for selected candidates and is not suitable or accessible for all patients.²⁴

Consequently, there remains a clear therapeutic gap in the management of obesity-related asthma. A pharmacologic intervention that addresses both airway inflammation and systemic metabolic dysfunction would represent a significant advancement.

GLP-1 RAs: Mechanisms of action and clinical utility

GLP-1 is a gut-derived incretin hormone that enhances insulin secretion, inhibits glucagon release, delays gastric emptying, and promotes satiety. GLP-1 RAs, including liraglutide, semaglutide, and tirzepatide (a dual GLP-1/glucose-dependent insulinotropic polypeptide agonist), are approved for the treatment of T2DM and obesity due to their efficacy in promoting weight loss and reducing cardiometabolic risk.²⁵

Importantly, GLP-1 receptors (GLP-1Rs) are expressed beyond the pancreas, including in the lungs, vasculature, and immune cells, suggesting pleiotropic effects that may extend to respiratory diseases.

Potential mechanisms of benefit in asthma

GLP-1 RAs may improve asthma control through the following:

Anti-inflammatory effects

Preclinical studies in mice have demonstrated that GLP-1 RAs reduce lung levels of IL-6, TNF-α, and other inflammatory mediators. They also inhibit nuclear factor-kappa B (NF-κB) activation, a key transcription factor in inflammatory signaling.²⁶

Reduction in airway hyperresponsiveness (AHR)

GLP-1 RAs have been shown to attenuate AHR in animal models, potentially by reducing oxidative stress and airway inflammation.²⁷ GLP-1R protein expression is markedly increased in the lung, particularly in pulmonary epithelial and endothelial cells, suggesting a critical role in lung function.²⁸ Previous studies have also highlighted the potential of GLP-1R activation in modulating airway function. In ex vivo models, exendin-4, a GLP-1 RA, induced a bronchorelaxant effect when GLP-1R was activated.²⁹

Modulation of immune and airway smooth muscle (ASM) cells

GLP-1 RAs act on ASM cells by reducing their proliferation, migration, and secretion of inflammatory mediators. These effects are mediated through upregulation of adenosine triphosphate-binding cassette transporter A1 (ABCA1) and suppression of pro-inflammatory cytokines, including IL-6, IL-8, TNF-α, and granulocyte–macrophage colony-stimulating factor (GM-CSF).³⁰ GLP-1 RAs also inhibit the formation of asymmetric dimethylarginine (ADMA) by modulating advanced glycation end products (AGEs) and their interaction with the receptor for AGE (RAGE).³¹ These effects are mediated via protein kinase A (PKA) activation and suppression of NF-κB, leading to decreased expression of protein arginine methyltransferase 1 (PRMT1) and reduced production of reactive oxygen species. Consequently, endothelial nitric oxide synthase (eNOS) activity, which is normally inhibited by ADMA, is enhanced, contributing to improved endothelial function and reduced inflammation.²⁸

GLP-1 RAs, such as semaglutide, have been shown to modulate immune cell activity, potentially shifting the immune balance away from a pro-inflammatory phenotype.³² This effect is mediated through modulation of dendritic cells, macrophages, and T cells, influencing their signaling pathways and cytokine production.³³ GLP-1 RAs can alter responses to inflammatory stimuli. For example, they can inhibit the production of pro-inflammatory cytokines, such as TNF-α and IL-6, by macrophages, while promoting the production of anti-inflammatory cytokines such as IL-10, resulting in a shift toward an anti-inflammatory macrophage phenotype.³⁴ GLP-1 RAs may also modulate T-cell responses, potentially reducing the activity of pro-inflammatory Th1 and Th17 while promoting the activity of anti-inflammatory subsets (Th2 and regulatory T cells). By influencing these key immune cell populations, GLP-1 RAs contribute to a broader shift in the immune system away from a pro-inflammatory state, which may be beneficial in conditions characterized by chronic inflammation, such as T2DM and cardiovascular disease.³¹

Improvement in lung mechanics

Weight loss achieved through GLP-1 RAs has been shown to improve lung function and reduce respiratory symptoms. Specifically, studies have demonstrated that GLP-1 RAs, frequently used to treat T2DM and promote weight loss, can increase lung volumes, reduce airway closure, and enhance spirometry outcomes.³⁵ These effects may lead to reduced dyspnea (shortness of breath) and improvements in overall quality of life, particularly in individuals with obesity and related respiratory conditions.

Insulin sensitization

By improving insulin sensitivity, GLP-1 RAs may reduce insulin-driven ASM proliferation and remodeling.³⁶ Hyperinsulinemia associated with insulin resistance has been identified as a stronger risk factor than body mass for the development of asthma. Recent studies indicate that insulin resistance contributes to airway remodeling, ASM proliferation, increased airway contractility and hyperresponsiveness, and the release of pro-inflammatory mediators from adipose tissue.³⁷ Collectively, these effects underscore the impact of hyperinsulinemia on airway structure and function and support the concept of a distinct asthma phenotype associated with insulin resistance.

Clinical evidence supporting GLP-1 RAs in asthma

Retrospective data

A large retrospective cohort study by Foer et al.³⁸ examined over 5000 adults with asthma and T2DM. Patients treated with GLP-1 RAs had significantly lower asthma exacerbation rates compared with those receiving other diabetes medications. These effects appeared to be independent of weight loss and glycemic control, supporting a potential direct anti-inflammatory role. Another study of 10,111 individuals exposed to GLP-1 RAs in the Optimum Patient Care Research Database (OPCRD) reported improved symptom control and weight loss compared with non-exposed patients.³⁹

Observational studies

Patients with obesity and asthma who achieved >10% weight loss through GLP-1 RAs reported improved asthma control scores and reduced need for rescue inhalers. Improvements in lung function, including forced expiratory volume in 1 second (FEV₁) and forced vital capacity, have also been documented.⁴⁰

Ongoing clinical trials

A randomized controlled trial (RCT), the GATA-3 study, is currently underway to investigate treatment with semaglutide in symptomatic asthma associated with obesity, a difficult-to-treat patient population (Table 2). This proof-of-concept, double-blind, placebo-controlled, single-site RCT will enroll adult patients (aged ≥ 18 years, n = 100) with obesity (BMI ≥ 30 kg/m²) and symptomatic asthma without T2DM. This study aims to assess asthma symptoms, quality of life, and airway function to evaluate the effect of semaglutide on asthma control. In addition, markers of respiratory tract inflammation and adipose tissue will be monitored to determine the impact of semaglutide on lower airway inflammation (https://clinicaltrial.be/en/details/32273).

Table 2.

Proposed clinical profile for GLP-1 RA candidacy in asthma management.

Characteristic	Rationale	Clinical assessment
Obesity (BMI ≥30 kg/m²)	Addresses a root metabolic driver of the asthma phenotype	BMI measurement
Poor asthma control	Targets an unmet clinical need in patients uncontrolled on standard ICS/LABA therapy	ACQ, ACT, exacerbation history
Metabolic dysfunction	The drug’s primary mechanism directly targets insulin resistance or metabolic syndrome	HbA1c, fasting glucose/insulin, lipid profile
Late-onset, non-T2 phenotype	Patients with pauci-granulocytic or neutrophilic inflammation may benefit most due to limited efficacy of T2-targeted biologics	Sputum/blood eosinophils, FeNO
SAD	Addresses a key “treatable trait” in obese asthma that may improve with weight reduction and metabolic changes	Oscillometry

GLP-1 RA: glucagon-like peptide-1 receptor agonist; BMI: body mass index; ACQ: Asthma Control Questionnaire; ACT: Asthma Control Test; FeNO: fractional exhaled nitric oxide; HbA1c: hemoglobin A1c (glycated hemoglobin); ICS: inhaled corticosteroids; LABA: long-acting beta-2 agonist; SAD: small airway dysfunction; T2: type 2.

Safety and tolerability

GLP-1 RAs are generally well tolerated. Common adverse effects include nausea, vomiting, and diarrhea, particularly during dose escalation. Although the risk of pancreatitis is low, it remains a concern in susceptible individuals. Importantly, these agents have demonstrated cardiovascular benefits in high-risk populations, including reductions in major adverse cardiac events.⁴¹

Future directions and research priorities

Although preliminary data are promising, the following questions remain unresolved:

Which asthma phenotypes benefit most? Likely those with obesity, non-T2 inflammation, insulin resistance, and metabolic syndrome.

What is the role in non-obese asthma? Currently unknown; benefits in lean individuals are likely limited to metabolic overlap.

What biomarkers can guide therapy? Identifying responders based on inflammatory profiles, adipokines, or genetic markers will be essential.

Can the use of techniques such as oscillometry to identify SAD early be useful in an integrated diagnostic work-up? Recent studies show that patients with moderate to severe asthma and obesity have significantly worse oscillometry-defined SAD, despite type 2 inflammation, spirometry, asthma control, and exacerbation frequency being similar to non-obese patients with asthma.⁴² Cluster analysis incorporating oscillometry identified older, obese, and female patients as being at greater risk for poor future asthma control.

Can GLP-1 RAs be combined with other asthma therapies? Combination with ICS, biologics, or bronchial thermoplasty may yield synergistic effects.

What is the impact of GLP-1 RAs on muscle adiposity? Lower paraspinal muscle density, indicative of higher fat infiltration, has previously been shown to be an independent factor associated with worse SAD in women with asthma as well as airway remodeling.^43,44

What is the impact of GLP-1 RAs on body composition? Although weight loss is a primary benefit, concerns about sarcopenia (muscle loss) are emerging. Understanding the effects on both fat mass and lean muscle mass—particularly paraspinal muscle, which is linked to airway dysfunction—is crucial for long-term health.^45,46

Conclusion

The intersection of obesity and asthma presents an increasing challenge in modern clinical medicine. As the field moves beyond an airway-centric model of asthma care, there is growing recognition of the need to address systemic contributors to large and small airway disease, including adipose-driven inflammation, insulin resistance, and altered immune regulation.

GLP-1 RAs offer a unique and timely opportunity to bridge this gap. By targeting both the metabolic and immunological abnormalities of obesity-associated asthma, they have the potential to transform the therapeutic landscape for this difficult-to-treat population (Figure 1 and Table 3). As ongoing clinical trials generate additional data, it is plausible that GLP-1 RAs will become part of an integrated, precision-medicine approach to asthma management.

Figure 1.

The obesity–asthma link and the emerging role of GLP-1 RAs. GLP-1 RAs: glucagon-like peptide-1 receptor agonists; IL-6: interleukin-6; TNF-α: tumor necrosis factor-alpha; non-T2: non type 2; OSA: obstructive sleep apnea; GERD: gastroesophageal reflux disease.

In future studies, it will be important to determine whether patients with coexisting asthma and obesity, with or without T2DM, experience improved control and pulmonary function of the large and small airways with therapies such as the GLP-1 RA semaglutide. Future investigations could also stratify FEV₁ trajectories to identify distinct phenotypes of decline and to select the most appropriate treatment options, including GLP-1 RAs, based on asthma endotype and comorbidities, including the increasingly prevalent obesity (Table 4).

Table 3.

Summary of proposed benefits of GLP-1 RAs in obesity-associated asthma.

Proposed mechanism	Evidence	Potential clinical relevance
Anti-inflammatory effects	Reduced IL-6 and TNF-α in preclinical models; decreased systemic inflammation in humans	May reduce airway and systemic inflammation
Immune modulation	Downregulation of NF-κB signaling; altered macrophage and T-cell responses	Improved immune balance; possible efficacy in non-T2 asthma
Reduction in AHR and mucus secretion	Animal studies show decreased methacholine responsiveness and airway mucin production	May improve symptoms and reduce exacerbation frequency
Weight loss and improved lung mechanics	10%–15% mean weight reduction in clinical trials	Improves lung volumes, dyspnea, and asthma control
Insulin sensitization	Reversal of hyperinsulinemia in obese subjects	May prevent airway remodeling and fixed airflow limitation
Improved cardiovascular/metabolic health	Lower blood pressure, lipids, and cardiovascular events in large RCTs	Reduces systemic risk and supports overall asthma management goals

GLP-1 RAs: glucagon-like peptide-1 receptor agonists; IL-6: interleukin-6; TNF-α: tumor necrosis factor-alpha; NF-κB: nuclear factor kappa B; AHR: airway hyperresponsiveness; T2: type 2; RCTs: randomized controlled trials.

Table 4.

Ideal patient profile for GLP-1 RA therapy in asthma.

Characteristic	Ideal candidate profile
Primary diagnosis	Patients with symptomatic asthma and coexisting obesity (BMI ≥30 kg/m²)
Asthma phenotype/endotype	Late-onset obesity-related asthma Often non-eosinophilic, less allergic, neutrophilic, or pauci-granulocytic May present with a shift from Th2 (eosinophilic) to Th1 or Th17 (neutrophilic) inflammation Likely with non-T2 inflammation
Clinical course and severity	Patients with difficult-to-treat asthma Asthma that is more severe and difficult to control Characterized by poor asthma control and increased risk of exacerbations
Response to standard therapies	Poor or blunted responsiveness to standard therapies, especially ICS Those where high-dose ICS/LABA combinations ma provide limited benefit
Associated metabolic conditions	Patients with metabolic dysfunction Presence of insulin resistance Diagnosed with metabolic syndrome
Other comorbidities	Individuals with overlapping symptoms from comorbidities such as OSA and GERD
Lung function profile	Patients with SAD, which may be disproportionate to spirometry findings Can be identified using techniques such as oscillometry
Inflammatory markers	Greater expression of neutrophils, IL-17A, and IL-25 mRNA in sputum Characterized by chronic, low-grade systemic inflammation with increased levels of IL-6 and TNF-α

GLP-1 RA: glucagon-like peptide-1 receptor agonist; BMI: body mass index; Th: T helper; T2: type 2; ICS: inhaled corticosteroids; LABA: long-acting beta-2 agonist; OSA: obstructive sleep apnea; GERD: gastroesophageal reflux disease; SAD: small airway dysfunction; IL: interleukin; mRNA: messenger ribonucleic acid; TNF-α: tumor necrosis factor-alpha.

Footnotes

Acknowledgments

None.

Author contributions

FM conceptualized and planned the article and drafted the manuscript. MC and RC contributed to the review and editing of the manuscript. All authors read and approved the final version.

AI tools

During the preparation of this article, the authors used Gemini Pro to enhance the clarity and readability of the language. After using this tool, the authors carefully reviewed and edited the content and take full responsibility for the final version of the manuscript.

Data availability statement

Not applicable, as this is a narrative review.

Declaration of conflicting interests

FM has received research funding from AstraZeneca, GlaxoSmithKline, Chiesi Farmaceutici, and Sanofi and fees as a speaker/lecturer from AstraZeneca, Chiesi Farmaceutici, GlaxoSmithKline, Sanofi, Merck, and Insmed. MC reports personal fees for talks from Chiesi, Menarini, and GlaxoSmithKline, as well as support for attending meetings from Chiesi. RC reports institutional grants from Chiesi, AstraZeneca, and GlaxoSmithKline; advisory board participation for AstraZeneca; personal fees from AstraZeneca (talks and drafting educational material), Chiesi (talks), Thorasys (talks), and Vitalograph (drafting educational materials); and support for attending meetings from AstraZeneca, Chiesi, NIOX, Sanofi-Regeneron, and Vitalograph.

Funding

The authors received no financial support for the research, authorship, or publication of this article.

ORCID iD

Francesco Menzella

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