- Article
- Source: Campus Sanofi
- May 15, 2024
Role of type 2 Inflammation
Type 2 Inflammation may increase the risk of exacerbations and lung function impairment in COPD23,24
COPD is characterized by mucus production, airway obstruction, and coughing13
Inflammation manifests systemically and locally
- Chronic inflammation causes structural changes, including narrowing of the airways and decreased lung elasticity13
- Studies have identified a relationship between inflammation and mucus hypersecretion in respiratory conditions such as COPD25
Listen to Prof Nicola Hanania : “We no longer look at it as a one-size-fits-all disease”
1:36 minutes
Nicola Hanania is Professor of Medicine, Section Chief of Pulmonary Critical Care and Sleep Medicine at the Ben Taub Hospital in Houston, Texas, and Director of the Airways Clinical Research Center, ACRC, at the Bear College of Medicine.
Listen to the whole episode of the podcast on the EMJ website
Sponsored by Sanofi and Regeneron, in partnership with EMJ.
I think our approach to this all disease has changed, knowing that it has multiple what we call phenotypes, but also not only that, but we have identified multiple mechanism of the disease, so we no longer look at it as a one-size-fits-all disease. And so therefore it's very important for clinician to do some really digging deep into history to identify these phenotypes, whether it's a frequent exacerbative phenotype, whether it's a chronic bronchitic phenotype, whether it's an emphysema mainly phenotype, but now we use biomarkers like blood eosinophils and maybe more to come, including radiology biomarkers in the future, may help us subdivide this group of patients so that we can do a more personalized approach. And I think it's very exciting time for COPD, so we have moved from this blue-bloater pink puffer type approach to now having multiple, as I mentioned, subtypes or phenotypes, and including the identifying more mechanism so that we have more targeted approach to this disease. And hopefully that will help improve outcomes in the future, obviously. That's the main goal is to move that increased risk of mortality that we have seen in COPD, while we have seen so much achievement with other diseases in COPD. Unfortunately, we haven't moved that envelope a lot, so I think we're hoping with new approaches we may improve outcomes.
Look for elevated blood eosinophils (>300 Cells/Lμ) - A Biomarker of Type 2 Inflammation in COPD13
Elevated eosinophils in COPD are a treatable trait and marker of type 2 inflammation13
The 2024 GOLD Report recognizes elevated blood EOS as a clinically used biomarker in identifying COPD with type 2 inflammation
Type 2 inflammation in COPD can involve multiple pathways, cytokines, and inflammatory cells28-33
IL-4, IL-13, an IL-5 are type 2 cytokines involved in COPD
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aBased on findings from 5 studies in COPD patients without asthma. Eosinophil levels used to define type 2 inflammation ranged from ≥300 cells/μL to ≥340 cells/μL (blood), ≥2% in induced sputum or 3% in peripheral blood. Percentages of patients with type 2 inflammation ranged from 12.3% to ~40%23,24
bA severe exacerbation was defined as a hospitalization due to COPD. Exacerbations had to be a minimum of 4 weeks apart to be considered separate exacerbations.27
cIn a cohort of patients with EOS >200 cells/μL.26
dReproduced with permission of the American Thoracic Society. Fritzsching B et al. Am J Respir Crit Care Med. 2015;191(8):902-91325
eAlcian blue PAS staining of mucus in airway epithelial cells.25
fResults from an observational study of 1553 patients with GOLD spirometry grade 2-4 COPD (postbronchodilator FEV1/FVC ratio <0.7, with FEV, >80% predicted)23
gResults from a 1-year observational study of 479 patients with COPD, 173 of whom had blood eosinophil levels ≥200 cells/μL and/or ≥2% of the total white blood cell count.24
COPD, chronic obstructive pulmonary disease; EOS, eosinophils; FEV1, forced expiratory volume in 1 second; FVC, forced vital capacity; GOLD, Global Initiative for Chronic Obstructive Lung Disease; IFN-y, interferon-gamma; ILC2, innate lymphoid type-2 cells; MUC5AC, mucin 5AC; PAS, periodic acid-Schiff; TNF-a, tumor necrosis factor alpha; TSLP, thymic stromal lymphopoietin.
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