Speaker's Highlight

• Don Sin University of British Columbia, St. Paul Hospital (Canada)
  Kenneth R. Chapman Toronto General Hospital Research Institute (Canada)
• Parameswaran Nair McMaster University (Canada)
  Carolyn Calfee UCSF (U.S.A.)
• Gregory P. Downey University of Colorado School of Medicine (U.S.A.)
  David A. Schwartz University of Colorado School of Medicine (U.S.A.)
• Neil Schluger Tuberculosis Control Branch, California Department of Public Health (U.S.A.)
  Nick Kim Critical Care & Sleep Medicine, University of California San Diego (U.S.A.)
• Nicola Hananiah Baylor College of Medicine (U.S.A.)
  Jae-Joon Yim Seoul National University College of Medicine (Republic of Korea)
• Koichiro Asano Tokai University School of Medicine (Japan)
  Diahn-Warng Perng Taipei Veterans General Hospital (Taiwan)
• Konstantinos Kostikas University of Ioannina (Greece)
  Karin Klooster University Medical Center Groningen (Kingdom of the Netherlands)

• Understanding eosinophilic asthma and targeted treatments

  Asthma is a diverse respiratory disease rather than a single condition. Some people have airway inflammation driven largely by eosinophils, a type of white blood cell involved in allergic and immune responses. This pattern is often called eosinophilic asthma and may occur with or without obvious allergies.

  The condition can begin in childhood or adulthood, and symptoms may remain difficult to control even when inhaled treatment is used correctly. Frequent wheezing, coughing, chest tightness, nighttime symptoms, and repeated exacerbations can indicate that the inflammatory process needs closer evaluation.

  Advances in respiratory medicine have made it possible to match treatment with biological features. Understanding blood eosinophils, fractional exhaled nitric oxide, immunoglobulin E, lung function, and exacerbation history helps clinicians decide whether a targeted therapy could reduce attacks and improve daily control.

  What eosinophilic inflammation means

  Eosinophils can migrate into the bronchial walls and release substances that cause swelling, mucus production, and increased airway sensitivity. This immune activity is commonly linked with type 2 inflammation, which may also involve interleukin-4, interleukin-5, interleukin-13, and thymic stromal lymphopoietin.

  The eosinophilic pattern is not defined by one universal test result. Eosinophil counts can change over time and may be lowered by oral corticosteroids. A person may also have overlapping allergic and eosinophilic features, while some patients with high eosinophils do not experience severe asthma.

  Severity and control are different concepts. Asthma may be classified as severe when substantial treatment is needed to maintain control, while poor control can result from incorrect inhaler technique, missed doses, smoking exposure, chronic sinus disease, obesity, or another diagnosis.

  Recognizing the clinical pattern

  Possible clues include repeated asthma attacks requiring systemic steroids, persistent symptoms despite medium- or high-dose inhaled corticosteroids, adult-onset disease, nasal polyps, chronic rhinosinusitis, and fluctuating airflow obstruction. Some patients have little day-to-day allergy history but still show strong eosinophilic activity.

  A careful clinical review is essential because breathlessness and cough can also arise from vocal cord dysfunction, bronchiectasis, chronic obstructive pulmonary disease, heart disease, reflux, or infection. Spirometry with bronchodilator testing helps confirm variable airflow limitation, while peak-flow monitoring can reveal changes over time.

  Treatment response also provides useful information. Fewer exacerbations, improved lung function, reduced reliever use, and lower steroid requirements suggest better control, although symptom scores and objective testing should be considered together.

  Confirming type 2 airway disease

  A blood eosinophil count is convenient and widely available, but its interpretation depends on timing, previous corticosteroid exposure, infections, and laboratory variation. Sputum eosinophils can offer a more direct view of airway inflammation, although this test is not available in every clinic.

  Fractional exhaled nitric oxide, or FeNO, can support the assessment of type 2 airway inflammation. Raised FeNO may indicate corticosteroid-responsive inflammation, but it can also be influenced by allergic rhinitis, smoking, recent medication use, and adherence. Total IgE and specific allergy testing are particularly useful when considering an anti-IgE treatment.

  Before escalation, clinicians generally review inhaler technique, prescription collection, treatment adherence, comorbidities, and environmental triggers. These steps prevent a treatable management problem from being mistaken for treatment-resistant disease.

  Targeted medicines and treatment selection

  Biologic medicines work by interrupting specific immune signals. They are usually considered for severe asthma that remains uncontrolled despite optimized inhaled therapy, especially when exacerbations or long-term oral steroid use create significant health risks.

  The best option depends on the patient’s inflammatory profile, age, comorbid conditions, dosing preferences, local approval criteria, and previous response. Biomarkers guide selection, but they do not replace clinical judgment.

  Treatment pathway	Main target	Features that may support consideration
  Anti-IgE therapy	Immunoglobulin E	Allergic asthma, sensitization to relevant allergens, suitable IgE range, and exacerbation risk
  Anti-IL-5 therapy	Interleukin-5	Raised blood eosinophils and recurrent exacerbations
  Anti-IL-5 receptor therapy	IL-5 receptor on eosinophils	Eosinophilic inflammation with frequent attacks or steroid dependence
  Anti-IL-4 receptor therapy	IL-4 and IL-13 signaling	Type 2 inflammation, raised FeNO, eosinophilia, or steroid-dependent asthma
  Anti-TSLP therapy	Thymic stromal lymphopoietin	Severe uncontrolled asthma across a broader range of inflammatory patterns

  Biologics are add-on therapies, not substitutes for prescribed inhaled corticosteroids unless a specialist directs a change. Their goal may include fewer severe attacks, improved lung function, better symptom control, and reduced exposure to oral corticosteroids.

  Monitoring response and safety

  Evaluation should continue after treatment begins. Clinicians may review exacerbation frequency, asthma control questionnaires, lung function, reliever use, FeNO, blood eosinophils, and the need for oral steroids. A meaningful response can involve fewer attacks even if symptoms do not disappear completely.

  Adverse effects vary by medicine. Injection-site reactions and headache are relatively common with some biologics, while hypersensitivity reactions are uncommon but clinically important. Patients should follow the prescribed observation and emergency guidance, particularly after initial doses.

  Stopping or switching a biologic should be a planned specialist decision. Treatment intervals, insurance requirements, vaccination status, pregnancy considerations, parasitic infection risk, and coexisting nasal polyps may all affect the management plan.

  Building a reliable control strategy

  Targeted therapy works best as part of a broader asthma program. Patients benefit when they understand their action plan, recognize early deterioration, and know when reliever use or symptoms require urgent medical assessment.

  Practical priorities include:

  • Use the prescribed inhaler with a technique checked regularly by a clinician or pharmacist.
  • Record exacerbations, steroid courses, night waking, reliever use, and possible triggers.
  • Treat related conditions such as allergic rhinitis, chronic sinus disease, nasal polyps, reflux, or sleep-disordered breathing when clinically appropriate.
  • Avoid tobacco smoke and reduce occupational or household exposures that worsen airway symptoms.
  • Attend follow-up visits so biomarkers, lung function, and biologic response can be reviewed together.

  The aim is durable control with the lowest effective medication burden. A personalized plan also helps distinguish temporary symptom changes from a genuine need to adjust therapy.

  Respiratory specialists, primary care teams, pharmacists, and patients each contribute to successful asthma management. Discuss persistent symptoms or repeated attacks with a qualified clinician, request an assessment of inhaler use and inflammatory markers, and use specialist guidance to determine whether targeted treatment is appropriate for your clinical profile.

  Richard Russell Nuffield Department of Clinical Medicine, University of Oxford (United Kingdom)
• Mona Bafadhel King’s College London (United Kingdom)
  David Jackson Guy’s and St Thomas’ Hospital, King’s College London (United Kingdom)
• James Chalmers University of Dundee (United Kingdom)
  David Price University of Aberdeen (United Kingdom)