ArticleMultidisciplinary respiratory medicine2025
Neutrophil dysfunction in bronchiectasis: Pathophysiological insights and emerging targeted therapies.
Article in Multidisciplinary respiratory medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bronchiectasis is a heterogeneous, chronic airway disease characterized by irreversible bronchial dilation, persistent infection, and neutrophilic inflammation. As traditional treatments often fail to address the underlying pathophysiology, particularly the central role of dysfunctional neutrophils, this review explores recent advances in the understanding of neutrophil-driven mechanisms in bronchiectasis and highlights emerging targeted therapies for this condition. A comprehensive literature review of studies published between 2020 and 2025 focusing on neutrophil activity, biomarkers, and clinical trials evaluating novel anti-inflammatory agents for the treatment of bronchiectasis was conducted. Data were synthesized from experimental models, randomized controlled trials (WILLOW and ASPEN), and expert consensus guidelines (ERS 2023-2024). These results indicate that neutrophils contribute to tissue destruction in bronchiectasis via serine proteases and excessive neutrophil extracellular trap (NET) formation. Key emerging therapies include DPP-1 inhibitors (e.g., brensocatib), CXCR2 antagonists, PI3K inhibitors, and NET-targeting therapies. Biomarkers, such as neutrophil elastase activity, sputum procalcitonin, and NMR-derived metabolic phenotypes, may help personalize therapy, and combination treatment strategies alongside precision medicine are reshaping the therapeutic landscape of ABPA. Although targeting neutrophil dysfunction offers a promising avenue for advancing bronchiectasis care, balancing immunomodulation and infection control remains a challenge. The integration of novel therapies with biomarker-guided treatment and treatable trait approaches is essential to improve the outcomes of this complex disease.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.