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Bronchoalveolar lavage proteomics in exacerbation of bronchiectasisopen access

Authors
Lee, Ju YeonYang, JiyoulKim, Jin YoungDo, YejiKim, Min-SikKye, Dong EunMin, GeonhuiJeon, In-SookKim, Eung-GookChoi, Joong KookChoi, MinjaeLee, HyunYang, Bumhee
Issue Date
Oct-2025
Publisher
BioMed Central
Keywords
Bronchiectasis; Bronchoalveolar lavage; Proteomics; Neutrophil degranulation
Citation
BMC Pulmonary Medicine, v.25, no.1, pp 1 - 10
Pages
10
Indexed
SCIE
SCOPUS
Journal Title
BMC Pulmonary Medicine
Volume
25
Number
1
Start Page
1
End Page
10
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/209142
DOI
10.1186/s12890-025-03904-6
ISSN
1471-2466
Abstract
BackgroundThe molecular pathophysiology underlying the development of bronchiectasis with exacerbation at the proteomic level has not been clarified using bronchoalveolar lavage fluid samples. This study aimed to evaluate the bronchoalveolar lavage fluid inflammatory profiles associated with exacerbation of bronchiectasis.MethodsWe analyzed the bronchoalveolar lavage fluid specimens from 4 patients in the exacerbation status and 4 patients in a stable status using liquid chromatography-tandem mass spectrometry.ResultsA total of 1,577 proteins were identified using proteomic analysis, with 127 differentially expressed proteins. Of 127 differentially expressed proteins, 23 proteins showed more than 2-fold differences between exacerbation and stable status groups. The exacerbation status was associated with 18 upregulated proteins (TPI1, CRP, BPI, ORM1, PTPRE, S100A9, BPY2, TPM4, ERVFC1-1, CYS1, CLEC3B, S100A8, PSAT1, NDUFA10, MDGA1, SPRR3, ALDOA, and PSMB2) and five downregulated proteins (MUC5B, HSPE1, KLK13, IGHA1, and MUC5AC). Pathway analysis revealed that the neutrophil degranulation pathway (R-HSA-6798695) was the most enriched pathway in these proteins, followed by the C-type lectin receptor pathway (R-HSA-5621481).ConclusionThe bronchoalveolar lavage fluid protein expression in patients in the exacerbation status of bronchiectasis was significantly different from that in patients in the stable status, indicating that neutrophil degranulation and C-type lectin receptor pathways are the most enriched pathways during exacerbation.
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