Given that severe asthma management is entering a new era of biologically driven precision, Dr. Sally Wenzel joins us to discuss the complexity within Type 2 inflammation and the limitations of relying on a single biomarker assessment. She also differentiates childhood-onset allergic asthma from adult-onset disease, underscoring how age of onset—along with underlying biology—can inform therapeutic strategy. Dr. Wenzel serves as the Director of the Asthma Institute at UPMC, and she spoke about this topic at the 2026 American Academy of Allergy, Asthma, and Immunology Annual Meeting.
How Biologic Insights Are Refining Severe Asthma Care

Announcer:
This is Clinician’s Roundtable on ReachMD, and on this episode, we’ll hear from Dr. Sally Wenzel. Not only does she serve as the Director of the Asthma Institute at UPMC, but she’s also the Chair for the Department of Environmental and Occupational Health at the University of Pittsburgh’s School of Public Health. She’ll be sharing highlights from her presentation at the 2026 American Academy of Allergy, Asthma, and Immunology Annual Meeting, which focused on the latest biological insights and the future of precision medicine in severe asthma. Let’s hear from Dr. Wenzel now.
Dr. Wenzel:
Now we have two different types of asthma. We have Type 2 high asthma, which is identified by elevations in blood eosinophils and elevations in exhaled nitric oxide—those are the two most commonly used biomarkers—compared to those who don't have elevations in those biomarkers who we call Type 2 low. But really, we don't have a biomarker to identify those people; it's just the absence of the Type 2 biomarkers.
I think the main evolving points are number one, people have suggested that the vast majority of severe asthma may end up being Type 2 low and that there's not as many Type 2 high patients. But I think that comment or question requires a deeper dive. And certainly, we know that if you measure Type 2 biomarkers—blood eosinophils and exhaled nitric oxide—repeatedly, many patients who were not elevated in those biomarkers will be become elevated with repeated measurements. We also know that inhaled and oral corticosteroids typically suppress these biomarkers. So if you have someone who is on inhaled corticosteroids, which most asthma patients are and should be by the time they are identified as a severe asthma patient, the biomarkers can be suppressed because of the treatment, but that doesn't mean that the entire Type 2 biology that may be underlying their disease is actually gone. So I think that's a really critical point to emphasize.
And then the other point to emphasize is that even when people have Type 2 high asthma identified by those two biomarkers, it doesn't mean that all Type 2 high asthma is the same. You have some patients who will do incredibly well on a Type 2 biologic and other people who will not do very well, and you'll have some patients who will do well on a specific biologic who won't do well on a similar Type 2 pathway biologic that doesn't treat their Type 2 disease. So there's nuance here.
It's not just Type 2 high asthma. There are subtypes of Type 2 high asthma. The majority of people with Type 2 high asthma probably have an allergic early onset disease, and we've known for close to a hundred years that there's a difference between asthma that you get in childhood versus asthma that you get in adulthood. And I think many people underappreciate how many people get asthma as an adult and that asthma as an adult seems to have a different pattern, so it's not as allergic as the childhood onset disease—typically, not always, but typically. And so asking a patient when they got their disease or when they developed symptoms is actually a really important aspect to understand about their disease.
If they got their disease in childhood, typically they will have this allergic type of disease that can be responsive to various biologics including, omalizumab anti-IgE, anti-TSLP or thymic stromal lymphopoietin, and certainly anti-IL4 receptor antibodies as well. All of those seem to do a pretty good job of inhibiting allergic responses. And then of course, you've got the other side of the coin, which is the adult-onset patients often who have high levels of Type 2 inflammation. And there I think your options are perhaps a little bit broader in that there's good data to support the efficacy of the anti-IL5 pathway blockers. There's also very good evidence to support anti-IL4 receptor antibodies and anti-TSLP antibodies as well.
So I think going beyond just Type 2 inflammation and trying to identify the types of Type 2 asthma that the patient has is a very important next step. And then make sure that you've measured these Type 2 biomarkers enough times to truly understand whether they do or do not have elevation in these biomarkers.
Announcer:
That was Dr. Sally Wenzel talking about her presentation at the 2026 American Academy of Allergy, Asthma, and Immunology Annual Meeting on how emerging biological insights are shaping precision medicine in severe asthma. To access this and other episodes in our series, visit Clinician’s Roundtable on ReachMD.com, where you can Be Part of the Knowledge. Thanks for listening!
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Overview
Given that severe asthma management is entering a new era of biologically driven precision, Dr. Sally Wenzel joins us to discuss the complexity within Type 2 inflammation and the limitations of relying on a single biomarker assessment. She also differentiates childhood-onset allergic asthma from adult-onset disease, underscoring how age of onset—along with underlying biology—can inform therapeutic strategy. Dr. Wenzel serves as the Director of the Asthma Institute at UPMC, and she spoke about this topic at the 2026 American Academy of Allergy, Asthma, and Immunology Annual Meeting.
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