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Illustration of stacked books representing scientific publications, educational resources, and COPD research for healthcare professionals.

Resources

Explore the latest in COPD science
  • Home
  • Burden of COPD
  • Inflammation in COPD
  • Mucus dysfunction in COPD
  • IL-33 in COPD
  • Resources

Publications

Publication on COPD exacerbations in patients receiving inhaled triple therapy
Publication on COPD exacerbations in patients receiving inhaled triple therapy

Burden of COPD

For many people with COPD, the burden of moderate and severe exacerbations persists despite inhaled triple therapy

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Congresses

ERS 2025 COPD symposium review and video resources
ERS 2025 COPD symposium review and video resources

IL-33 Is Not Just IL-33

An ERS 2025 symposium review article by EMJ

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ERS 2025 COPD symposium review and video resources
ERS 2025 COPD symposium review and video resources

ERS symposium videos

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Materials

IL-33 in COPD

Image outlining the role of IL-33 in COPD pathogenesis

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Video featuring experts discussing the history of IL-33 in COPD
Video featuring experts discussing the history of IL-33 in COPD

IL-33: A history video

History of IL-33 in COPD

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Disclaimer

This resource section includes links to peer-reviewed open-access articles. Copyright remains with the authors and/or publishers, as stated in each article. Any reused material is presented in accordance with the applicable license. 

Some publications may include discussion of investigational or unapproved products.

IL-33 in COPD

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Frequently asked questions

Illustration of lungs representing IL-33 signalling in COPD
Illustration of lungs representing IL-33 signalling in COPD

What does ‘dysregulated IL-33’ mean?

IL‑33 is released upon stress or cell damage to initiate a host response—what was adaptive turns maladaptive or ‘dysregulated’ when its levels chronically surpass buffering mechanisms and signalling is persistent1–8

Illustration of a person coughing, representing the impact of smoking on IL-33 signalling in COPD
Illustration of a person coughing, representing the impact of smoking on IL-33 signalling in COPD

How does smoking affect the IL-33 pathway in patients with COPD?

In COPD, smoking status affects the IL‑33 axis—former smokers show elevated IL-33 compared to current smokers, while current smokers show reduced sST2 and more oxidized IL‑33, indicating aberrant IL‑33–ST2 signalling in both groups9–12

Illustration of lungs representing the role of IL-33 in COPD inflammation
Illustration of lungs representing the role of IL-33 in COPD inflammation

How does the role of IL-33 in COPD differ from other epithelial cytokines?

Damage to the epithelium triggers the release of upstream, alarmin cytokines. IL-33 is pre-formed, rapidly released and initiates a broad inflammatory cascade encompassing Type 1, Type 2 and Type 3 responses1,13,14

Illustration of airways and alveoli representing IL-33 signalling in COPD
Illustration of airways and alveoli representing IL-33 signalling in COPD

What evidence would suggest my patient with COPD has dysregulated IL-33 signalling?

Frequent exacerbations, productive cough and persistent airway/systemic inflammation may suggest heightened IL‑33

pathway activity15–17

Illustration of lungs representing the consequences of dysregulated IL-33 signalling in COPD
Illustration of lungs representing the consequences of dysregulated IL-33 signalling in COPD

What are the potential consequences of dysregulated IL-33 signalling?

IL-33 through its dual forms can drive Type 1 and 3 and Type 2 (eosinophilic, subset) inflammation, and mucus dysfunction, which are key drivers of COPD pathogenesis1–3,12,15

Illustration of mucus representing mucus dysfunction in COPD
Illustration of mucus representing mucus dysfunction in COPD

What is mucus dysfunction and what is the impact for patients with COPD?

Mucus dysfunction is the pathological changes in mucus volume, composition and clearance, the airway manifestations of these pathological changes, and the downstream

clinical consequences12,15,18–25

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  1. Cayrol C. Cells. 2021;11(1):107
  2. Calderon AA, et al. Eur Respir Rev. 2023;32(167):220144
  3. Brightling CE, et al. Eur Respir J. 2019;54(6):1900651
  4. England E, et al. Sci Rep. 2023;13(1):9825
  5. Rabe KF, et al. Am J Respir Crit Care Med. 2023;208(4):395–405
  6. Keddache S, et al. Clin Immunol. 2021;229:108798
  7. Scott IC, et al. Biochem Soc Trans. 2018;46(5):1345–1353
  8. Burgoyne RA, et al. Cells. 2021;10(10):2763
  9. Abdo M, et al. Eur Respir J. 2024;64(3):2400347
  10. Faiz A, et al. Am J Respir Crit Care Med. 2023;208(10):1075–1087
  11. Faiz A, et al. Am J Respir Crit Care Med. 2023;208(Suppl.):1075–1087
  12. Strickson S, et al. Eur Respir J. 2023;62(3):2202210
  13. Cayrol C, Girard JP. Cytokine. 2022;156:155891
  14. Varricchi G, et al. Eur Respir J. 2024;63(4):2301619
  15. Diaz AA, et al. JAMA. 2023;329(21):1832–9
  16. Shen Y, et al. Int J Chron Obstruct Pulmon Dis. 2018;13:399–407
  17. Rodrigues SO, et al. Pharmaceuticals (Basel). 2021;14(10):979
  18. Fahy JV, Dickey BF. N Engl J Med. 2010;363(23):2233–2247
  19. Stott-Miller M, et al. Int J Chron Obstruct Pulmon Dis. 2020;15:2467–2476
  20. Hughes R, et al. Respir Med. 2022;200:106921
  21. Choate R, et al. Chronic Obstr Pulm Dis. 2020;7(1):49–59
  22. Cook N, et al. Int J Chron Obstruct Pulmon Dis. 2019;14:1365–1376
  23. Tian PW, Wen FQ. J Transl Int Med. 2015;3(3):89-92
  24. Mettler SK, et al. N Engl J Med. 2025;392(19):1973–1975
  25. Zhou D, et al. Expert Rev Respir Med. 2025:1–7

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