Asthma endotypes in flux: integrating type 1 and type 2 inflammation for biological therapy advancement.
Level 5 - mechanism / opinion, no new human data
Narrative literature review summarizing mechanisms, biomarkers, and clinical trials without systematic synthesis or quantitative meta-analysis.
PubMed 40884772 · doi:10.1080/02770903.2025.2555300
What was done
The authors conducted a literature review searching PubMed, Embase, Cochrane databases, trial registries, and regulatory agency documents. They evaluated literature on type 1 (T1) and type 2 (T2) asthma immunopathology, biomarker development, and biological therapies, prioritizing randomized controlled trials, systematic reviews, and large observational studies.
What was found
The abstract provides a qualitative overview without reporting quantitative data. T2 inflammation (involving IL-4, IL-5, IL-13, and eosinophils) has established biomarkers (blood eosinophils, FeNO, periostin) and effective targeted biologics (anti-IL-5, anti-IL-4Rα, anti-IgE). In contrast, T1 inflammation (involving IFN-γ, TNF-α, IL-17, and neutrophils) lacks validated biomarkers and effective targeted therapies. The authors report that emerging evidence shows substantial T1/T2 overlap in severe asthma.
Why it matters
It highlights that severe asthma frequently involves mixed inflammatory endotypes rather than strict dichotomy, pointing toward upstream cytokine inhibition and multi-target strategies for precision therapy.
Limits
As a narrative review, it lacks a formal systematic review protocol, risk-of-bias grading, and quantitative meta-analysis. The abstract provides no specific study count, sample sizes, effect sizes, or standardized clinical criteria for defining mixed endotypes.