Abstract
Many patients with idiopathic pulmonary fibrosis (IPF) show lymphoplasmacellular infiltrates within lung peribronchovascular regions, but its relevance in lung fibrogenesis is still poorly defined. In two models of adenoviral TGF-β1 or bleomycin (BLM)-induced experimental lung fibrosis, we found significant accumulations of B cells interfused with T cells within the peribronchovascular compartment, along with significantly increased lung collagen deposition, lung histopathology and worsened lung function in WT mice. Importantly however, B cell deficient µMT KO mice similarly responded with lung tissue remodeling and worsened lung function upon either AdTGF-β1 or BLM treatment as WT mice. Comparative transcriptomic profiling of sorted B cells collected from lungs of AdTGF-β1 or BLM-exposed WT mice signified 449 commonly regulated genes with significant enrichment observed for gene ontology terms (GO terms) apparently not related to lung fibrogenesis. Collectively, in two experimental models of lung fibrosis, comparative analysis of characteristic lung fibrosis measures between WT and B cell-deficient mice did not support a major involvement of B cells in lung fibrogenesis in mice.
Footnotes
Cite this article as: European Respiratory Journal 2021; 58: Suppl. 65, PA2380.
This abstract was presented at the 2021 ERS International Congress, in session “Prediction of exacerbations in patients with COPD”.
This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).
- Copyright ©the authors 2021