Eosinophilic asthma is a type of severe asthma characterized by abnormally high levels of a specific type of white blood cell, called an eosinophil, in the airways, lungs, and blood. While everyone has eosinophils as a normal part of their immune system, in people with this condition, the body produces them in vast excess, and they accumulate in the lungs, driving a unique and powerful form of inflammation.

To understand this, it helps to think of your immune system as an army with different types of soldiers trained for specific missions. Eosinophils are like a highly specialized special forces unit. Their normal job is to fight off certain types of infections, particularly parasitic worms, and they also play a role in allergic reactions. In a healthy response, these “soldiers” are deployed in controlled numbers to fight a specific enemy.

In eosinophilic asthma, the immune system’s command center goes haywire. It deploys massive numbers of these eosinophil soldiers into the lungs even when there is no parasite to fight. These cells, primed for battle, release their payload of toxic granules and inflammatory chemicals directly into the airway tissues. This causes significant “collateral damage,” leading to:

• Chronic and severe airway inflammation.
• Swelling and damage to the airway lining.
• Excessive mucus production.
• Airway hyperresponsiveness (twitchy, irritable airways).

This intense, eosinophil-driven inflammation is what makes this type of asthma so severe and often resistant to standard treatments like inhaled corticosteroids. Eosinophilic asthma is considered a “Type 2” inflammatory disease, a category of immune dysfunction that also includes conditions like atopic dermatitis (eczema), nasal polyps, and allergic rhinitis.

In my experience, patients with eosinophilic asthma often say, “I’ve had asthma for years, but lately nothing seems to work.” That’s usually a red flag for this more stubborn subtype.

Eosinophilic asthma is caused by an overactive immune response that leads to elevated eosinophils in the lungs and bloodstream. Unlike typical allergic asthma, which is triggered by external allergens like pollen or dust mites, eosinophilic asthma is often driven by an internal, self-perpetuating inflammatory cycle.

The central players in this cycle are a group of signaling molecules called cytokines. In particular, a cytokine called Interleukin-5 (IL-5) acts like a powerful general for the eosinophil army. The immune system produces too much IL-5, which then sends out three critical commands:

1. It signals the bone marrow to produce more eosinophils.
2. It activates these eosinophils, getting them ready for battle.
3. It helps them survive longer in lung tissue.

Other cytokines, like IL-4 and IL-13, also play a key role in the Type 2 pathway, contributing to mucus production and airway twitchiness. This understanding of the specific molecules driving the inflammation has been the key to developing the new, targeted biologic therapies used to treat the disease.

Clinically, I always suspect eosinophilic asthma when patients don’t have classic allergy symptoms but still struggle with wheezing, coughing, and breathlessness that worsens over time.

Eosinophilic asthma typically develops later in life often after age 30 and doesn’t always follow the same patterns as childhood or allergic asthma.

• Adult-Onset: Unlike classic allergic asthma which often begins in childhood, eosinophilic asthma most frequently develops in adulthood, typically between the ages of 35 and 60.
• Often Non-Allergic: While some people with eosinophilic asthma also have allergies, many do not. For these individuals, the inflammation is not driven by a reaction to an external allergen but by the body’s own internal immune dysregulation.
• Genetic Predisposition: There is likely a genetic component that makes some individuals more prone to developing this type of Type 2 inflammatory response, but specific genes are still being identified.
• Association with Other Conditions: A person is at higher risk of having eosinophilic asthma if they also have other conditions driven by the same inflammatory pathway. The most common of these is chronic rhinosinusitis with nasal polyps, a condition causing severe, persistent sinus inflammation and growths inside the nose.

Patients often say, “I never had asthma as a kid,” and I explain that eosinophilic asthma is different, it can appear out of the blue and behave very differently than childhood asthma.

While the symptoms of eosinophilic asthma can resemble classic asthma, they are often more severe, more persistent, and less responsive to usual treatment.

The classic asthma symptoms include:

• Shortness of breath
• Wheezing (a whistling sound when breathing)
• Chest tightness or pressure
• Chronic cough

However, there are several features that are more characteristic of the eosinophilic subtype and should raise suspicion:

• Severe and Persistent Symptoms: The asthma is often severe and does not respond well to standard high-dose inhaled corticosteroids.
• Frequent Asthma Attacks: Individuals often experience frequent and severe exacerbations (asthma attacks) that require treatment with oral corticosteroids (like prednisone) or even hospitalization.
• Chronic Sinus Problems: A history of chronic sinusitis, a poor sense of smell, and particularly the presence of nasal polyps are very strong clues.
• Adult Onset: The asthma symptoms began in adulthood rather than childhood.
• Normal Allergy Tests: The person may have severe asthma symptoms but test negative for common environmental allergies.

Clinically, I’ve seen patients come in frustrated after months of flare-ups. The key is recognizing the pattern, frequent, stubborn symptoms plus high eosinophil counts signal it’s time for specialized care.

Diagnosis

The journey to a diagnosis of eosinophilic asthma begins with a diagnosis of asthma itself, usually based on symptoms and breathing tests like spirometry. However, when a patient’s asthma is severe or doesn’t respond to standard therapy, a specialist (usually a pulmonologist or an allergist/immunologist) will investigate further to see if it is a specific subtype.

The key to diagnosing eosinophilic asthma is to measure the number of eosinophils. This can be done in several ways:

• Blood Eosinophil Count: This is the simplest and most common test. A standard complete blood count (CBC) with a differential can measure the number of eosinophils circulating in the blood. A count above a certain threshold (e.g., 150 to 300 cells per microliter) suggests the presence of eosinophilic inflammation (American Lung Association, 2023).
• Sputum Eosinophil Count: This is a more direct but less commonly available test. The patient coughs up a sample of phlegm (sputum), which is then examined under a microscope to count the percentage of eosinophils directly from the airways.
• Fractional Exhaled Nitric Oxide (FeNO) Test: This is a simple, non-invasive breathing test. The patient exhales into a device that measures the level of nitric oxide, a gas that is often elevated in people with Type 2 inflammation.
• Bronchial Biopsy: In some cases, a doctor may perform a bronchoscopy to take a small tissue sample (biopsy) from the airway lining to directly count the eosinophils, but this is an invasive procedure and not routinely done for diagnosis.

A doctor will use a combination of these test results along with the patient’s clinical history (adult onset, nasal polyps, frequent exacerbations) to make a confident diagnosis of severe eosinophilic asthma.

I often explain that eosinophilic asthma is not just “regular asthma” that’s gotten worse, it’s a different process, and testing helps us tailor the right treatment.

Treatment

Eosinophilic asthma typically does not respond well to regular inhaled corticosteroids alone. Advanced treatments are aimed at targeting eosinophil levels and reducing airway inflammation.

1. Standard Asthma Therapy: The foundation of treatment remains standard asthma care, which includes a high-dose inhaled corticosteroid (ICS) combined with a long-acting beta-agonist (LABA). However, in many people with eosinophilic asthma, this is not enough to control the inflammation.

2. Oral Corticosteroids (OCS): Before the advent of newer therapies, many patients with severe eosinophilic asthma were “steroid-dependent.” They required frequent or even daily courses of oral steroids like prednisone to manage their symptoms. While effective at dampening inflammation, long-term use of OCS can cause serious side effects, including weight gain, diabetes, osteoporosis, cataracts, and an increased risk of infection. A major goal of modern therapy is to reduce this OCS burden.

3. Biologic Therapies (Targeted Treatment): This is the revolutionary breakthrough in the treatment. Biologics are not pills or simple inhalers; they are monoclonal antibodies, which are lab-engineered proteins designed to find and block a specific molecule in the inflammatory pathway. They are given as an injection or infusion every few weeks.

These drugs work by targeting the specific drivers of the eosinophilic inflammation:

• Anti-IL-5 Therapies: These drugs (mepolizumab, reslizumab, and benralizumab) directly target Interleukin-5, the “general” that commands the eosinophil army. By blocking IL-5 or its receptor, these medications prevent the production and activation of eosinophils, dramatically reducing their numbers in the blood and lungs.
• Anti-IL-4/IL-13 Therapies: One drug (dupilumab) works by blocking the receptors for two other key cytokines in the Type 2 pathway, IL-4 and IL-13. This helps reduce both eosinophilic inflammation and other features of Type 2 inflammation, like mucus production.
• Anti-IgE Therapy: For patients who have both eosinophilic asthma and a strong allergic component, a drug called omalizumab, which targets the allergy antibody IgE, may be used.

These biologic therapies have been shown in clinical trials to significantly reduce asthma exacerbations, improve lung function, and, crucially, allow many patients to reduce or completely stop taking oral corticosteroids (AAAAI, 2020). However, they are highly specialized and expensive medications, and access can be a significant consideration depending on the healthcare system and insurance coverage.

I’ve seen biologics change lives, patients who once needed monthly ER visits are now stable, with fewer symptoms and better control. The key is identifying the right time to escalate care.

Eosinophilic asthma is a distinct and severe subtype of asthma that is defined by its underlying biology, an overabundance of inflammatory eosinophils. For too long, patients with this condition struggled, their symptoms poorly controlled by standard therapies and their health impacted by the heavy burden of oral steroid use. The scientific breakthroughs that have illuminated the role of the eosinophil and the Type 2 inflammatory pathway have paved the way for a new era of treatment. With a proper diagnosis confirmed by simple blood or breathing tests, patients can now access highly effective biologic therapies that target the root cause of their inflammation. Patients often tell me the diagnosis was a turning point, finally understanding their symptoms weren’t “just asthma,” but something more complex that needed a new approach.

American Academy of Allergy, Asthma & Immunology (AAAAI). (2020). Eosinophilic asthma: AAAAI expert tips. Retrieved from https://www.aaaai.org/tools-for-the-public/conditions-library/asthma/eosinophilic-asthma-expert-tips

American Lung Association. (2023). Eosinophilic asthma. Retrieved from https://www.lung.org/lung-health-diseases/lung-disease-lookup/asthma/learn-about-asthma/eosinophilic-asthma

Mayo Clinic. (2023). Eosinophilic asthma. Retrieved from https://www.mayoclinic.org/diseases-conditions/eosinophilic-asthma/symptoms-causes/syc-20452586