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Review
. 2024 Jul 3;33(173):230234.
doi: 10.1183/16000617.0234-2023. Print 2024 Jul.

Biomarkers in bronchiectasis

Affiliations
Review

Biomarkers in bronchiectasis

Emma Johnson et al. Eur Respir Rev. .

Abstract

Bronchiectasis is a heterogeneous disease with multiple aetiologies and diverse clinical features. There is a general consensus that optimal treatment requires precision medicine approaches focused on specific treatable disease characteristics, known as treatable traits. Identifying subtypes of conditions with distinct underlying biology (endotypes) depends on the identification of biomarkers that are associated with disease features, prognosis or treatment response and which can be applied in clinical practice. Bronchiectasis is a disease characterised by inflammation, infection, structural lung damage and impaired mucociliary clearance. Increasingly there are available methods to measure each of these components of the disease, revealing heterogeneous inflammatory profiles, microbiota, radiology and mucus and epithelial biology in patients with bronchiectasis. Using emerging biomarkers and omics technologies to guide treatment in bronchiectasis is a promising field of research. Here we review the most recent data on biomarkers in bronchiectasis.

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Conflict of interest statement

Conflict of interest: E. Johnson has nothing to disclose. M.B. Long reports travel support from the British Thoracic Society, Asthma+Lung UK and the American Thoracic Society, outside the submitted work. J.D. Chalmers reports grants from AstraZeneca, Genentech, Gilead Sciences, GlaxoSmithKline, Insmed, Grifols, Novartis and Boehringer Ingelheim; and consulting fees from AstraZeneca, Chiesi, GlaxoSmithKline, Insmed, Grifols, Novartis, Boehringer Ingelheim, Pfizer, Janssen, Antabio and Zambon, all outside the submitted work.

Figures

FIGURE 1
FIGURE 1
Established and exploratory biomarkers related to each aspect of the bronchiectasis vicious vortex: inflammation, infection, epithelial dysfunction and impaired mucociliary clearance, and structural lung damage. Established biomarkers are shown in bold. NETs: neutrophil extracellular traps; PZP: pregnancy zone protein; SLPI: secretory leukocyte protease inhibitor; TNF: tumour necrosis factor; IL: interleukin; FENO: exhaled nitric oxide fraction; CRP: C-reactive protein; ESR: erythrocyte sedimentation rate; MMP: matrix metalloproteinase; P. aeruginosa: Pseudomonas aeruginosa; R. mucilaginosa: Rothia mucilaginosa; HRCT: high-resolution computed tomography; MRI: magnetic resonance imaging; PET: positron emission tomography; CT: computed tomography. Reproduced and modified from [5] with permission. Figure created with biorender.com.
FIGURE 2
FIGURE 2
Known interactions between biomarkers of neutrophilic inflammation, infection, epithelial dysfunction and mucociliary clearance in bronchiectasis. MMP: matrix metalloproteinase; SLPI: secretory leukocyte protease inhibitor; AAT: alpha-1 antitrypsin; NETs: neutrophil extracellular traps; NE: neutrophil elastase; PR: proteinase; MPO: myeloperoxidase; PZP: pregnancy zone protein; AZU: azurocidin; ICAM: intracellular adhesion molecule; LTB4: leukotriene B4; TNF: tumour necrosis factor; IL: interleukin. Figure created with biorender.com.
FIGURE 3
FIGURE 3
High-resolution computed tomography findings associated with different bronchiectasis aetiologies, and with treatment response. a) Localised bronchiectasis affecting the lingula and left lower lobe (with previous left lower lobectomy) due to severe childhood infection; b) bilateral lower-lobe bronchiectasis with mucus plugging, worse on the right with associated inflammatory nodules, in a patient with chronic aspiration due to previous oesophagectomy and gastric pull-up; c) middle-lobe varicose bronchiectasis with bronchial wall thickening and extensive mucus plugging due to primary ciliary dyskinesia; d) middle-lobe bronchiectasis with tree-in-bud nodularity due to Mycobacterium avium pulmonary disease; e) idiopathic bilateral lower lobe bronchiectasis with mucus plugging most marked in the left lower lobe due to Pseudomonas aeruginosa infection; f) improvement in appearance with reduced mucus plugging following nebulised colomycin to treat P. aeruginosa.

References

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