{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T11:21:33Z","timestamp":1787570493915,"version":"build-2736575974"},"reference-count":39,"publisher":"European Respiratory Society (ERS)","issue":"4","license":[{"start":{"date-parts":[[2026,4,9]],"date-time":"2026-04-09T00:00:00Z","timestamp":1775692800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100010564","name":"Deutsches Zentrum f\u00fcr Lungenforschung","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100010564","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["publications.ersnet.org"],"crossmark-restriction":true},"short-container-title":["ERJ Open Res"],"accepted":{"date-parts":[[2026,3,4]]},"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Fibroblasts are important contributors to collagen deposition in interstitial lung diseases (ILD), but their inflammatory role in acute exacerbation of ILD including idiopathic pulmonary fibrosis is currently undefined.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Using a well-described model of\n                      <jats:italic>Streptococcus pneumoniae-<\/jats:italic>\n                      induced exacerbation of lung fibrosis in mice, we found that platelet-derived growth factor receptor A-positive lung fibroblasts developed an early inflammatory phenotype upon infection, including increased production of serum amyloid A (SAA) proteins, as determined by RNA sequencing, single-cell RNA sequencing and secretome profiling of sorted lung fibroblasts.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Lung fibroblasts responded to pneumococcal challenge with increased SAA mRNA and protein levels\n                      <jats:italic>in vitro<\/jats:italic>\n                      . SAA levels were significantly elevated in bronchoalveolar lavage (BAL) and plasma of mice with\n                      <jats:italic>S. pneumoniae<\/jats:italic>\n                      -induced exacerbation of adenoviral vector delivery of active transforming growth factor-\u03b21- or bleomycin-induced lung fibrosis. Antibiotic therapy caused a significant drop in SAA levels in BAL and plasma of mice with infection-driven fibrosis exacerbation. Finally, levels of SAA protein were dramatically increased in plasma of patients with acute exacerbation of ILD, but not in patients without exacerbation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Analysis of plasma levels of SAA protein may aid in the identification of underlying inflammation in patients with ILD who are more likely to deteriorate towards a critical clinical stage during acute exacerbation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1183\/23120541.01320-2025","type":"journal-article","created":{"date-parts":[[2026,4,9]],"date-time":"2026-04-09T14:55:19Z","timestamp":1775746519000},"page":"01320-2025","update-policy":"https:\/\/doi.org\/10.1183\/ers-crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Lung fibroblasts contribute to release of serum amyloid A as potential biomarker of exacerbation of 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