Pathogenesis of bronchial asthma: how inflammation, bronchospasm, mucus, and remodeling trigger attacks

The pathogenesis of bronchial asthma is a chain of mechanisms that cause the airways to become inflamed, hypersensitive, and prone to sudden narrowing. In modern medicine, asthma is viewed not as a single symptom of "suffocation," but as a heterogeneous chronic disease in which inflammation, bronchial smooth muscle spasm, mucosal edema, viscous mucus production, and structural changes in the bronchial wall can occur in varying proportions in different patients. [1]

The World Health Organization describes asthma as a chronic lung disease in which inflammation and contraction of the muscles around the airways make breathing difficult. Symptoms include coughing, wheezing, shortness of breath, and chest tightness, and can be mild or severe and change over time. [2]

The main characteristic of asthma pathogenesis is variability. One person experiences an attack after exposure to pollen, another after a viral infection, and yet another after physical exertion, cold air, smoke, or an occupational irritant. But the end result is often similar: the bronchi narrow, inflammation in the airway walls increases, airflow becomes more difficult, and a feeling of shortness of breath develops. [3]

The current Global Initiative for Asthma 2026 strategy emphasizes that asthma is a heterogeneous disease typically associated with chronic airway inflammation. This means that different patients may have different immune mechanisms, different biomarkers, different treatment responsiveness, and different risk of exacerbations. [4]

The practical implications of understanding pathogenesis are very simple: if you treat only bronchospasm without addressing the inflammation, the disease remains active. This is why modern guidelines increasingly emphasize the need for access to anti-inflammatory inhalers for all people with asthma, not just rapid bronchodilators. [5]

Mechanism	What's happening	How does it manifest itself?
Inflammation of the respiratory tract	Immune cells and mediators maintain swelling and irritation of the bronchi	Cough, wheezing, night symptoms, exacerbations
Bronchospasm	The smooth muscles of the bronchi contract	Sudden shortness of breath, wheezing
Edema of the mucous membrane	The bronchial wall thickens and the lumen narrows.	It's harder to exhale, and the tightness in the chest increases.
Excess mucus	The glands and goblet cells secrete more fluid.	Cough, feeling of phlegm, blockage of small bronchi
Bronchial hyperreactivity	The bronchi overreact to common irritants.	Attacks after cold, odors, stress, infection
Remodeling	The bronchial wall gradually undergoes structural changes	More persistent airflow restriction

Table source: World Health Organization, Global Asthma Initiative, Review of Airway Hyperresponsiveness and Airway Epithelium. [6] [7]

Bronchial epithelium: the first line of defense and trigger for inflammation

The bronchial epithelium is a layer of cells lining the airways. While it was once often thought of as a passive "lining," it is now considered an active regulator of asthma: it recognizes viruses, allergens, smoke, air pollution, cold, and chemical irritants, then sends alarm signals to the immune system. [8]

When the epithelium is damaged, so-called alarmins—signaling molecules that alert the immune system to danger—are released. Key epithelial alarmins in asthma include thymic stromal lymphopoietin, interleukin-33, and interleukin-25; they help trigger type 2 inflammation by activating dendritic cells, innate lymphoid cells type 2, eosinophils, and other participants in the inflammatory response. [9]

This mechanism explains why asthma often begins or worsens after exposure to external irritants. For example, a viral infection or air pollution damages the epithelial barrier, the epithelium releases alarmins, the immune system becomes overactive, and the bronchi become swollen, sensitive, and prone to spasm. [10]

The epithelium is also involved in bronchial hyperreactivity. A recent review from 2024 emphasizes that structural changes in the airways and epithelial-derived mediators can enhance the tendency of the bronchi to overconstrict in response to irritants. This helps explain why, in a patient with asthma, ordinary cold air or a strong odor can trigger a severe attack. [11]

In severe asthma, the epithelium becomes not only a participant in inflammation but also a potential therapeutic target. Therefore, drugs that target epithelial alarmins, such as thymic stromal lymphopoietin blockade, are considered an important treatment option for severe asthma, especially when the disease is not fully explained by classic allergies. [12]

Epithelial mechanism	What launches	Consequences for the bronchi
Barrier damage	Viruses, allergens, smoke, air pollution	The bronchi become more vulnerable
Isolation of alarmins	Thymic stromal lymphopoietin, interleukin-33, interleukin-25	Triggering immune inflammation
Activation of dendritic cells	Presentation of the allergen to the immune system	Formation of an allergic response
Activation of innate lymphoid cells	Rapid inflammatory response without classic allergy	Eosinophilic inflammation and hyperreactivity
Impaired epithelial restoration	Repeated damage and incomplete repair	Airway remodeling
Signals to smooth muscles and fibroblasts	Inflammatory and growth mediators	Thickening of the bronchial wall

Source of table: reviews on alarmins and epithelial mechanisms of asthma. [13] [14]

Type 2 inflammation: allergy, eosinophils, and key interleukins

Type 2 inflammation is one of the most studied variants of asthma pathogenesis. It is often associated with allergies, eosinophils, immunoglobulin E, and the cytokines interleukin-4, interleukin-5, and interleukin-13. This variant is found in many patients with allergic asthma, but can also occur in non-allergic eosinophilic forms of the disease. [15]

Interleukin-4 helps the immune system switch to producing immunoglobulin E, which is involved in the allergic reaction. When the allergen re-enters the respiratory tract, immunoglobulin E can activate mast cells and basophils, which release mediators that cause bronchospasm, swelling, and increased mucus secretion. [16]

Interleukin-5 is particularly important for eosinophils. It supports their maturation, survival, and accumulation in the airways. Eosinophils secrete substances that damage the epithelium, promote inflammation, increase bronchial hyperreactivity, and may participate in bronchial remodeling. [17]

Interleukin-13 affects several key components of asthma: it increases mucus production, promotes bronchial hyperreactivity, is involved in epithelial changes, and can influence structural changes in the airways. Therefore, blocking the interleukin-4 and interleukin-13 pathways has become a modern approach to treating severe asthma with type 2 inflammation. [18]

Type 2 inflammation is important not only for theory but also for practice. Its characteristics help guide treatment: a physician can evaluate blood eosinophils, exhaled nitric oxide fraction, allergic sensitization, and immunoglobulin E levels to understand why asthma is poorly controlled and whether the patient is a candidate for biological therapy. [19]

Participant of type 2 inflammation	The main role	Clinical significance
Immunoglobulin E	Participates in allergic reactions	May be a target for anti-immunoglobulin therapy
Mast cells	Rapidly release bronchospasm mediators	Participate in early allergic reactions
Eosinophils	Support inflammation and damage to the epithelium	Associated with exacerbations and severe eosinophilic asthma
Interleukin-4	Supports the allergic immune response	Important for the production of immunoglobulin E
Interleukin-5	Supports eosinophils	Target of biological drugs
Interleukin-13	Increases mucus and hyperreactivity	Target therapy for type 2 inflammation
Fraction of nitric oxide in exhaled air	Reflects type 2 inflammation in the airways	Helps phenotype asthma

Source of table: reviews on type 2 inflammation and immunological mechanisms of asthma.[20] [21]

Non-Type 2 Inflammation: Neutrophils, Infections, Irritants, and Hard-to-Control Asthma

Not all asthma is allergic or eosinophilic. Some patients have non-type II inflammation: sputum and airways may have a predominance of neutrophils, a mixed cell composition, or, conversely, a paucity of granulocytes. These variants are less well-studied, more difficult to diagnose, and often respond less well to standard anti-inflammatory inhaled glucocorticosteroids. [22]

Non-type 2 asthma may be associated with chronic infections, air pollution, tobacco smoke, vaping, obesity, occupational irritants, airway aging, and other factors. Its mechanisms involve immune pathways involving T-helper cells type 1 and 17, interleukin-6, interleukin-17, neutrophil extracellular traps, and inflammasome activation. [23]

Neutrophilic asthma is especially important in severe and difficult-to-control cases. Neutrophils help fight infections, but when chronically activated, they can release enzymes, oxidative molecules, and signals that promote tissue damage, mucus hypersecretion, and persistent inflammation. [24]

Paucigranulocytic asthma is a variant in which there is no significant excess of either eosinophils or neutrophils in the airways. This does not mean the disease is absent: symptoms may be maintained by bronchial smooth muscle dysfunction, impaired neural regulation, airway remodeling, mechanical factors, and increased bronchial sensitivity. [25]

The practical challenge of non-type 2 asthma is that there are currently fewer accurate biomarkers and targeted treatments than for eosinophilic asthma. Therefore, physicians must carefully evaluate the diagnosis, inhalation technique, comorbidities, obesity, exposure to smoke, vaping, mold, air pollution, and occupational irritants. [26]

Variant of inflammation	Main signs	Potential clinical significance
Eosinophilic inflammation	Eosinophils, interleukin-5, and nitric oxide fraction are often elevated	Often responds better to type 2 anti-inflammatory drugs
Neutrophilic inflammation	Neutrophils, interleukin-17, infections, irritants	May be more difficult to control with standard therapy
Mixed granulocytic inflammation	There are both eosinophils and neutrophils	Often associated with a more severe course
Paucigranulocytic variant	There is no significant excess of eosinophils and neutrophils	Smooth muscle and remodeling may play a role
Poorly controlled asthma	Symptoms persist despite treatment	We need to look for correctable causes.
Severe asthma	Control is poor after treatment optimization	Specialized phenotyping is required

Source of table: reviews on non-type 2 asthma and immunological aspects of asthma. [27] [28]

Bronchospasm and bronchial hyperreactivity

Bronchospasm is a rapid contraction of the smooth muscles surrounding the bronchi. When the muscles contract, the bronchial lumen narrows, making airflow more difficult, especially when exhaling. A person experiences chest tightness, wheezing, and shortness of breath. The World Health Organization clearly states that asthma is associated not only with inflammation but also with muscle contraction surrounding the airways. [29]

Bronchial hyperreactivity means the airways overreact to stimuli that would cause minimal reaction in a healthy person. These can include cold air, physical exertion, dust, smoke, strong odors, laughter, a viral infection, or an allergen. The greater the hyperreactivity, the more easily an attack is triggered. [30]

In asthma, bronchial smooth muscle does not simply contract during an attack. With prolonged inflammation, it can increase in mass, become more active, and interact with immune cells, the epithelium, and the extracellular matrix. This links bronchospasm to longer-term airway remodeling. [31]

Bronchospasm explains why bronchodilators provide rapid relief during an attack. But it doesn't explain all of asthma. If a patient receives only a bronchial muscle relaxant, inflammation, epithelial damage, mucus production, and the risk of future exacerbations may persist. Therefore, modern strategies emphasize anti-inflammatory inhalers, not just "rescue" bronchodilators. [32]

Bronchial hyperreactivity may decrease with good inflammation control, but in some patients it persists due to structural changes in the bronchi, neural regulation, exposure to external stimuli, and remodeling. Therefore, asthma assessment should include not only the question "Are you currently experiencing an attack?" but also an analysis of triggers, symptom frequency, lung function, and response to anti-inflammatory treatment. [33]

Mechanism	What's happening	Why is this important for treatment?
Smooth muscle contraction	The bronchi narrow rapidly	Explains the rapid effect of bronchodilators
Hyperreactivity	The bronchi overreact to irritants	Explains attacks from cold, smells and stress
Edema of the bronchial wall	The lumen of the bronchus becomes narrower	Requires anti-inflammatory treatment
Mucus plugs	Air passes less well through the small bronchi.	May increase severe attacks
Increase in smooth muscle mass	The bronchial wall becomes more "compressible"	Associated with severe and chronic course
Epithelial mediators	Damaged epithelium increases the bronchial response	Maintains chronic hyperreactivity

Table source: World Health Organization, Review of Bronchial Hyperreactivity, Review of Airway Remodeling. [34] [35]

Mucus, swelling and blockage of small airways

In asthma, the bronchi narrow not only due to muscle spasms. The bronchial lining swells, inflammatory cells penetrate the airway wall, and glands and goblet cells begin to secrete more mucus. As a result, the bronchial lumen narrows for several reasons. [36]

Mucus in asthma often becomes thick and difficult to remove. It can form plugs that block the small airways. This is especially dangerous during severe exacerbations, when even intense breathing efforts fail to ensure normal airflow from the lungs. [37]

Interleukin-13 and other type 2 inflammatory mediators stimulate mucus production and epithelial remodeling to increase the number of mucus-producing cells. This explains why some patients with asthma experience not only shortness of breath but also a persistent cough, a sensation of phlegm, and difficulty clearing the airways. [38]

Small airways are particularly important because their narrowing can significantly impair ventilation, but is not always readily apparent during a routine examination. The patient may complain of shortness of breath and chest tightness, while between attacks, the physician may not hear any pronounced wheezing. Therefore, functional testing and symptom dynamics are more important than a single, "quiet" examination. [39]

Excess mucus also helps explain why a "silent lung" sometimes occurs during a severe attack: wheezing may decrease not because things are better, but because air is barely passing through severely narrowed or blocked bronchi. This condition requires immediate medical attention. [40]

Component of bronchial obstruction	What causes	Clinical manifestation
Smooth muscle spasm	Rapid narrowing of the bronchus	Wheezing, shortness of breath
Edema of the mucous membrane	Thickening of the bronchial wall	Tightness in the chest, difficulty exhaling
Thick mucus	Obstruction of small bronchi	Cough, phlegm, severe exacerbation
Goblet metaplasia	Increased number of mucus-producing cells	Chronic tendency to hypersecretion
Inflammatory cells	Damage to the epithelium and maintenance of edema	Nighttime symptoms and recurrent attacks
Narrowing of the small airways	Ventilation failure	Shortness of breath even with mild wheezing

Table source: World Health Organization, Type 2 Inflammatory Disease Review, Asthma and Allergy Foundation of America. [41] [42]

Bronchial remodeling: Why asthma may become more persistent

Airway remodeling is the structural reorganization of the bronchial wall during chronic inflammation and repeated injury. It may include thickening of the basement membrane, increased smooth muscle mass, growth of mucous glands, increased goblet cell numbers, vascular changes, and accumulation of extracellular matrix.[43]

This process is important because it can make obstruction less reversible. While at the onset of the disease, bronchial narrowing is primarily due to spasm and inflammatory edema, with prolonged and poorly controlled progression, some of the airflow restriction may be maintained by structural changes in the bronchial wall. [44]

The epithelium plays a significant role in remodeling. A 2024 review in the European Respiratory Journal emphasizes that the epithelium and epithelial cytokines are involved in initiating and maintaining structural changes in the airways. This links external irritants, inflammation, and long-term bronchial remodeling into a single chain. [45]

Remodeling does not necessarily develop uniformly in all patients. It is more often associated with a severe, prolonged, poorly controlled course, repeated exacerbations, and persistent inflammation. However, its elements can appear early, especially if asthma begins in childhood and remains poorly controlled for a long time. [46]

The practical conclusion: early control of inflammation is necessary not only to reduce current symptoms but also to reduce the risk of long-term structural changes. This is why current guidelines consider anti-inflammatory therapy a fundamental part of asthma management. [47]

Remodeling component	What's changing?	Possible consequence
Thickening of the basement membrane	The bronchial wall becomes denser	More persistent narrowing of the airways
Smooth muscle growth	The bronchus contracts more strongly and more easily	Increased bronchospasm
Increased goblet cells	More mucus-producing cells	Mucus plugs and cough
Growth of mucous glands	Increased secretion	More mucus and congestion
Vascular changes	More vessels and swelling	Thickening of the bronchial wall
Accumulation of extracellular matrix	Fibrous changes	Loss of elasticity and persistent obstruction

Source of table: reviews of airway remodeling in asthma.[48] [49]

Asthma flare-up: What happens during an attack?

An asthma exacerbation occurs when inflammation, bronchospasm, swelling, and mucus suddenly increase. Triggers can include a viral infection, allergen, air pollution, tobacco smoke, vaping, cold, exercise, stress, an occupational irritant, or discontinuing anti-inflammatory therapy. [50]

During an attack, the bronchi narrow, increasing resistance to airflow, especially during exhalation. Air is retained in the lungs, breathing quickens, the chest and neck muscles begin to work harder, and the patient feels unable to fully exhale and inhale again. [51]

In the early stages, a bronchodilator can quickly relieve some of the spasm. However, if the inflammation is severe, the mucosa is swollen, and the small bronchi are clogged with mucus, bronchodilation alone may not be enough. Therefore, anti-inflammatory medications are used for significant exacerbations, and severe attacks require medical attention. [52]

A severe exacerbation is dangerous because the respiratory system can become exhausted. A decrease in wheezing as the condition worsens is not always a good sign: if air barely passes, the wheezing may become quieter. Therefore, a clinical assessment of severity includes not only breath sounds but also speech, consciousness, oxygen saturation, respiratory rate, pulse rate, and lung function. [53]

Understanding the pathogenesis of exacerbations explains why modern strategies emphasize preventing attacks rather than simply stopping them. If a patient frequently requires a quick-relief medication, this means that inflammation and the risk of exacerbations are not adequately controlled. [54]

Attack stage	What's happening	What is dangerous?
Contact with trigger	An allergen, virus, smoke, cold or other irritant activates the bronchi.	Triggering an inflammatory response
Release of mediators	Mast cells, epithelia and other cells release signals	Spasm, swelling and mucus
Bronchospasm	Smooth muscles contract	Rapid shortness of breath and wheezing
Swelling and mucus	The lumen of the bronchus is further narrowed	The drug may not help completely
Air trap	Air is trapped in the lungs	Fatigue of the respiratory muscles
Severe exacerbation	Gas exchange is disrupted	Risk of respiratory failure

Table source: World Health Organization, Global Asthma Initiative, Asthma Pathophysiology Review. [55] [56]

Why pathogenesis is important for treatment selection

Asthma treatment works best when it addresses the underlying mechanisms of the disease. Bronchodilators relax smooth muscles and quickly reduce bronchospasm, but they do not eliminate chronic inflammation. Inhaled glucocorticosteroids reduce inflammation, hyperreactivity, and the risk of severe attacks. [57]

The Global Asthma Initiative 2026 emphasizes the urgent need for access to anti-inflammatory inhalers for all people with asthma. This reflects a key pathogenetic principle: asthma is an inflammatory disease, so treatment with only a fast-acting bronchodilator leaves the underlying disease uncontrolled. [58]

Biological therapy for severe asthma emerged precisely from an understanding of pathogenesis. If immunoglobulin E plays a leading role in a patient, anti-immunoglobulin therapy can be considered; if eosinophils and interleukin-5 are important, drugs against this pathway are used; if the interleukin-4 and interleukin-13 pathways are active, other biological targets are selected; if the epithelial alarmin thymic stromal lymphopoietin is important, therapy that affects the early onset of inflammation is possible. [59] [60]

However, pathogenesis cannot always be determined by symptoms. Two patients with the same dyspnea may have different mechanisms: allergic inflammation, eosinophilic asthma without overt allergy, neutrophilic inflammation, obesity-related asthma, occupational asthma, or severe remodeling. Therefore, in severe and uncontrolled cases, biomarkers and specialized assessment are needed. [61]

This is why modern medicine speaks not only of phenotypes, or visible clinical variants, but also of endotypes, or the internal mechanisms of the disease. This approach helps us not simply label asthma "severe," but rather understand why it is severe and what treatment approach makes the most sense. [62]

Pathogenetic target	Example of a mechanism	Therapeutic logic
Smooth muscles of the bronchi	Bronchospasm	Bronchodilators
Inflammation of the respiratory tract	Edema, hyperreactivity, exacerbations	Inhaled glucocorticosteroids
Immunoglobulin E	Allergic reaction	Antiimmunoglobulin therapy in appropriate patients
Interleukin-5 and eosinophils	Eosinophilic inflammation	Anti-eosinophilic biological therapy
Interleukin-4 and interleukin-13	Mucus, type 2 inflammation, hyperreactivity	Blockade of the relevant signaling pathways
Thymic stromal lymphopoietin	Early epithelial inflammatory signal	Blockade of epithelial alarmin
Remodeling	Structural reorganization of the bronchi	Early inflammation control and specialized management

Table source: Global Asthma Initiative, reviews on type 2 inflammation, alarmins, and immunological mechanisms of asthma. [63] [64]

Common misconceptions about the pathogenesis of asthma

The first misconception is that asthma is simply a spasm of the bronchi. Spasm is indeed important, but without inflammation, swelling, mucus, epithelial damage, and hyperreactivity, it is impossible to explain the chronic course, nocturnal symptoms, exacerbations, and the need for anti-inflammatory therapy. [65]

The second misconception is that asthma is always allergic. The allergic variant is common, but non-allergic, eosinophilic, neutrophilic, mixed, and paucigranulocytic variants also exist. Therefore, the absence of obvious allergy does not rule out asthma. [66]

The third misconception is that if attacks are infrequent, there is no inflammation. In practice, even patients with infrequent symptoms may be at risk of severe exacerbation, especially if they use only a fast-acting bronchodilator and do not receive anti-inflammatory protection. [67]

The fourth misconception is that sputum is a sign only of infection. In asthma, mucus can appear due to type 2 inflammation, the action of interleukin-13, irritation of the epithelium, and hypersecretion of the bronchial glands. Infection can be a trigger, but not the only explanation for mucus and cough. [68]

The fifth misconception is to consider severe asthma simply "severe allergies." Severe asthma may be associated with type 2 inflammation, but may also involve non-type 2 mechanisms, remodeling, obesity, infections, occupational exposures, improper inhalation technique, and comorbidities. [69]

Delusion	How to understand correctly
Asthma is just bronchospasm	This is inflammation, hyperreactivity, mucus, swelling and sometimes remodeling.
If there are no allergies, there is no asthma.	There are non-allergic and non-type 2 asthma variants.
If the symptoms are rare, there is no risk.	Rare symptoms do not exclude a severe exacerbation
Phlegm always means infection	Mucus may be part of asthmatic inflammation.
Salbutamol cures asthma completely	It dilates the bronchi, but does not treat inflammation.
Severe asthma is always the same	Severe asthma has different endotypes and requires phenotyping

Table source: World Health Organization, Global Asthma Initiative, reviews of immunological mechanisms of asthma. [70] [71]

FAQ

What is the main mechanism of bronchial asthma?

The primary mechanism of asthma is chronic inflammation of the airways, combined with bronchial hyperreactivity and reversible or partially reversible bronchial constriction. During symptoms, bronchospasm, mucosal edema, and increased mucus production are added. [72]

Why is it difficult to breathe out when you have asthma?

In asthma, the bronchi narrow, especially the small airways, making it harder for air to escape from the lungs. This creates an "air trap": a person has to exert more effort to exhale, and the next inhalation begins before the lungs are completely empty of air. [73]

What is type 2 inflammation?

Type 2 inflammation is an immune variant of asthma in which eosinophils, immunoglobulin E, interleukin-4, interleukin-5, and interleukin-13 are important. It is often associated with allergies, but can also occur without an obvious allergic trigger.[74]

What is non-type 2 asthma?

Non-type 2 asthma is a variant that lacks the prominent features of type 2 eosinophilic inflammation. It can be neutrophilic, mixed, or paucigranulocytic and is often more difficult to treat with standard treatment because there are fewer accurate biomarkers and targeted therapy options. [75]

Why does an allergen not trigger an attack in everyone at once?

The reaction depends on the sensitization of the immune system, the condition of the bronchial epithelium, the level of inflammation, the dose of the allergen, concomitant infection, therapy, and individual bronchial hyperreactivity. Therefore, the same allergen can cause a severe attack in one person and have little effect on another. [76]

Why does mucus appear during asthma?

Inflammatory mediators, especially in type 2 inflammation, stimulate mucus glands and goblet cells. This results in the production of thick mucus, which can increase coughing, a feeling of phlegm, and congestion of the small airways. [77]

What is bronchial remodeling?

Remodeling is a structural reorganization of the bronchial wall during chronic inflammation: tissue thickening, smooth muscle growth, enlargement of mucous cells, vascular changes, and accumulation of extracellular matrix. It can make respiratory limitation more persistent. [78]

Is it possible to stop remodeling completely?

Modern medicine cannot yet completely halt or reverse remodeling in all patients. However, good inflammation control, appropriate basic therapy, cessation of smoking and vaping, elimination of triggers, and treatment of severe asthma can reduce the risk of progression of structural changes. [79]

Why are inhaled corticosteroids so important?

They address the inflammatory basis of asthma, not just the symptom of bronchospasm. This is why the Global Asthma Initiative emphasizes the need for access to anti-inflammatory inhalers for all people with asthma. [80]

Why does a bronchodilator help quickly but not completely solve the problem?

A bronchodilator relaxes the smooth muscles of the bronchi and quickly makes breathing easier, but it does not eliminate chronic inflammation, epithelial damage, excess mucus, or the risk of future exacerbations. Therefore, it should not be the sole treatment strategy for asthma. [81]

Why does severe asthma require phenotyping?

Because severe asthma can be caused by a variety of mechanisms: allergic inflammation, eosinophilic inflammation, epithelial alarmins, neutrophilic inflammation, remodeling, comorbidities, or exposure to irritants. Phenotyping helps tailor treatment to the underlying mechanism. [82]

Why might asthma get worse after a viral infection?

Viruses damage the respiratory epithelium, increase the release of alarmins, activate the immune response, and increase bronchial hyperreactivity. Therefore, after an infection, the bronchi may remain sensitive for a longer period, even after the fever and main symptoms of a cold have passed. [83]

Key points from experts

Professor Helen K. Reddel, MD, PhD, Chair of the Scientific Committee of the Global Asthma Initiative, Macquarie University and the University of Sydney. The key practical message of current strategies is that asthma is a heterogeneous inflammatory disease, so it is necessary to assess not only symptoms but also the risk of exacerbations, inflammatory profile, inhalation technique, and response to anti-inflammatory treatment. [84]

Professor Guy Brusselle, Chairman of the Board of Directors of the Global Asthma Initiative, Ghent University, emphasized in 2026 that the preferred drug for symptom relief should be anti-inflammatory: it should quickly dilate the bronchi while simultaneously targeting the inflammation that underlies attacks. [85]

Professor Peter Bradding, a respiratory medicine specialist, authored a review on bronchial hyperreactivity and the role of the epithelium in asthma. His key scientific thesis is that bronchial hyperreactivity is not limited to smooth muscle contraction: the epithelium and structural changes in the airways actively support the bronchial overreaction to irritants. [86]

Professor Giorgio Varricchi, a researcher of airway inflammation and one of the authors of a review on airway remodeling in the European Respiratory Journal, shows that the epithelium and epithelial cytokines are involved not only in triggering inflammation but also in long-term structural remodeling of the bronchial wall. [87]

Professor Kian Fan Chung, National Heart and Lung Institute, Imperial College London, is an expert on severe asthma. The key practical principle of his work and international approaches to severe asthma is that before asthma is considered truly severe, the diagnosis must be confirmed, the inflammatory endotype must be assessed, and treatment errors and associated causes of poor control must be excluded. [88]

Result

The pathogenesis of bronchial asthma is not a single mechanism, but a complex network of processes: epithelial damage, alarmin release, type 2 or non-type 2 inflammation, bronchospasm, edema, mucus, hyperreactivity, and remodeling. These mechanisms are expressed differently in different patients, so asthma requires a personalized assessment. [89]

The most important practical implication is that asthma cannot be treated solely as a sudden bronchospasm. Rapid bronchodilation relieves an attack, but long-term control is achieved only when treatment addresses inflammation, reduces hyperreactivity, and reduces the risk of future exacerbations. [90]

A modern understanding of pathogenesis explains the emergence of biological therapy, phenotyping, and anti-inflammatory inhalers for symptom relief. The more accurately a physician understands the underlying mechanism of asthma in a particular patient, the greater the chance of selecting a treatment that not only relieves symptoms but also alters the course of the disease. [91]