
The airway epithelium is no longer understood as a passive wall. The panel traces how a barrier is now thought of as an immune organ, and what that shift means for severe asthma.
Expert pulmonologists and an allergist examine the evolving understanding of severe asthma and unified airway disease, including epithelial barrier dysfunction, epithelium-driven inflammation, and the upstream role of TSLP across diverse phenotypes. The panel reviews biomarkers, biologic selection, remission, and how integrated assessment and individualized strategies optimize outcomes in coexisting upper airway disease.

The airway epithelium is no longer understood as a passive wall. The panel traces how a barrier is now thought of as an immune organ, and what that shift means for severe asthma.

One cytokine sits above the rest. Dr. Hanania explains why TSLP earns the label of master regulator, and why blocking it reaches inflammation that current therapies cannot.

Phenotype, endotype, and treatable trait are used loosely and often interchangeably. The panel defines each term and tests where the boundaries between them break down.

A treatable trait is easier to endorse than to define. The panel works through what qualifies, and why extrapulmonary traits deserve the same attention as the airway itself.

Dr. Wechsler and Dr. Ross describe how they read overlapping results and what they weigh when no single marker dominates.

Alarmins are now leading therapeutic targets, yet no biomarker measures them. Dr. Hanania explains what blocking TSLP reveals downstream, and where the real measurement gap lies.

The assumption that anti-alarmin therapy is the answer for low T2 disease meets the trial evidence. Dr. Wechsler walks through where the efficacy signal actually concentrates.

Anatomy separated the sinuses from the lungs, and specialty training reinforced the split. The panel makes the case that the evidence describes a single organ with one disease process.

Not every patient with nasal polyps is allergic, and no test reliably separates those who are. The panel discusses how referral patterns skew what each specialist believes.

Biologics have displaced a procedure that once filled the fellowship schedule. The panel weighs what replaced aspirin desensitization, and how sinus surgery rates changed with it.

Seven approved agents across four targets, spanning two decades of approvals. Dr. Wechsler maps the class, then names the 40% of exacerbations it still does not prevent.

Evidence places biologics at GINA Step 5, and that is where reimbursement holds them. Dr. Hanania and Dr. Wechsler examine the case for moving earlier, and what it would require.

Clinicians define control as no exacerbations and no hospital stays. Dr. Ross argues patients define it differently, and that the gap between the two should drive treatment decisions.

With an anti-alarmin option that does not require a biomarker, selection could have become simpler. Dr. Hanania explains why it stays multifactorial, and why he waits before judging response.

Patients taper their own inhalers, and payers approve on exacerbations alone. The panel closes on where the evidence runs out and where documentation and advocacy take over.