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Decoding host-environment interactions in progressive pulmonary fibrosis: insights from hypersensitivity pneumonitis

dc.contributor.authorMeneses, Alexandra
dc.contributor.authorCardoso, Catarina G.
dc.contributor.authorCoelho, David B.
dc.contributor.authorMelo, Natália
dc.contributor.authorMota, Patrícia C.
dc.contributor.authorGuimarães, Susana
dc.contributor.authorMoura, Conceição S.
dc.contributor.authorCarvalho, André
dc.contributor.authorSokhatska, Oksana
dc.contributor.authorBeltrão, Marília
dc.contributor.authorDelgado, Luís
dc.contributor.authorMorais, António
dc.contributor.authorSaraiva, Margarida
dc.contributor.authorBastos, Hélder N.
dc.contributor.authorSantos, Rita F.
dc.date.accessioned2025-11-11T16:55:50Z
dc.date.available2025-11-11T16:55:50Z
dc.date.issued2025-05
dc.description.abstractInterstitial lung diseases (ILDs) comprise a heterogeneous group of parenchymal lung disorders characterized by diffuse infiltration of immune effector cells, fibroblasts, myofibroblasts, and extracellular matrix deposition at various pulmonary compartments. These conditions can progress to end-stage fibrosis, respiratory failure, and eventually, death. In 2020, we initiated the first national ILD registry and biobank under the FIBRALUNG project, which has enrolled over 950 cases to date, with over 40% of the cases being fibrotic ILDs. The most represented fibrotic ILD groups are Hypersensitivity Pneumonitis (HP) (46%), Idiopathic Pulmonary Fibrosis (IPF) (20%), and unclassifiable ILD (8%). HP is the leading cause of pulmonary fibrosis, nearly doubling the number of IPF cases, which contrasts with numbers from other countries. This underscores the importance of investigating non-IPF progressive pulmonary fibrosis within our setting. Longitudinal patient follow-up and biological sample collection were performed allowing patient stratification according to progression criteria. Our work so far has highlighted a potential role of CCL2-CCR2 axis in fibrotic HP disease progression. Elevated serum CCL2 strongly associated with disease progression and acute exacerbations, with baseline levels above 1080 pg/mL predicting oneyear progression/mortality. To complement these findings, we are conducting blood transcriptome analyses across different HP patient groups to identify progression-specific signatures. Simultaneously, lung microbiome profiling is underway to explore its role in fibrotic progression. These integrative approaches aim to uncover novel biomarkers and mechanistic pathways, paving the way for tailored therapeutic interventions.por
dc.identifier.citationMeneses, A., Cardoso, C. G., Coelho, D. B., Melo, N., Mota, P. C., Guimarães, S., Moura, C. S., Carvalho, A., Sokhatska, O., Beltrão, M., Delgado, L., Morais, A., Saraiva, M., Bastos, H. N., & Santos, R. F. (2025). Decoding host-environment interactions in progressive pulmonary fibrosis: Insights from hypersensitivity pneumonitis. Livro de Resumos do 18º Encontro de Investigação Jovem da U.Porto, 397–398. https://www.up.pt/ijup/wp-content/uploads/sites/892/2025/06/Livro-de-Resumos_IJUP-2025.pdf
dc.identifier.isbn978-989-746-418-8
dc.identifier.urihttp://hdl.handle.net/10400.22/30830
dc.language.isoeng
dc.peerreviewedyes
dc.publisherUniversidade do Porto
dc.relation.hasversionhttps://www.up.pt/ijup/wp-content/uploads/sites/892/2025/06/Livro-de-Resumos_IJUP-2025.pdf
dc.rights.uriN/A
dc.subjectPulmonary fibroses
dc.subjectHypersensitivity pneumonitis
dc.subjectBiomarkers
dc.subjectCCL2
dc.titleDecoding host-environment interactions in progressive pulmonary fibrosis: insights from hypersensitivity pneumonitispor
dc.typeconference paper
dspace.entity.typePublication
oaire.citation.conferenceDate2025-05
oaire.citation.conferencePlacePorto
oaire.citation.endPage398
oaire.citation.startPage397
oaire.citation.titleLivro de Resumos do 18º Encontro de Investigação Jovem da U.Porto
oaire.versionhttp://purl.org/coar/version/c_970fb48d4fbd8a85

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