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Investigation of CD64+ macrophages in bleomycin treated lungs [NGS2117]

ABSTRACT: Investigation of the comparative transcriptional signatures of CD64+ vs alveolar macrophages at different phases (day 5 and day 14) in the bleomycin-induced model of lung fibrosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE262965 | GEO | 2026/01/06

REPOSITORIES: GEO

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Investigation of CD64+ macrophages in bleomycin treated lungs [NGS2117]

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Depletion of club cells attenuates bleomycin-induced lung injury and fibrosis in mice

Project description:Background and objective: The role of bronchiolar epithelial cells in the pathogenesis of pulmonary fibrosis has not been addressed. We previously demonstrated that DNA damage was found in bronchiole at early phase, and subsequently extended to alveolar cells at later phase in bleomycin-induced pulmonary fibrosis in mice. Club cells are progenitor cells for bronchiole, and are recognized to play protective roles against lung inflammation and damage. The aim of the study was to elucidate the role of club cells in the development of pulmonary fibrosis. Methods: C57BL/6J mice were received naphthalene intraperitoneally at day -2 to deplete club cells, and were given intratracheal bleomycin or vehicle at day 0. Lung tissues were obtained at day 1, 7, and 14, and bronchoalveolar lavage was performed at day 14. Gene expression was analysed from bronchiolar ephithelial cells sampled by laser captured microdissection at day 14. Results: Surprisingly, naphthalene-induced club cell depletion protected mice from bleomycin-induced lung injury and fibrosis. We conclude that club cells are involved in the development of lung injury and fibrosis.

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Multiple bleomycin exposed mouse lung epithelial type 2 cells

Project description:We analyze the mRNA level in multiple PBS or bleomycin exposed mouse lung alveolar epithelial type 2 cells

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Transciptional profile of pericytes and stromal cells in bleomycin lung injury

Project description:We previously showed that pericyte-like cells derived from the FoxD1-lineage contribute to myofibroblasts following bleomycin-induced lung injury. However, their functional significance in lung fibrosis remains unknown. In this study, we used a model of lung pericyte-like cell ablation to test the hypothesis that pericyte-like cell ablation attenuates lung fibrosis in bleomycin-induced lung injury. Methods: Lung fibrosis was induced by intratracheal instillation of bleomycin. To ablate pericyte-like cells in the lung, diphtheria toxin (DT) was administered to Foxd1-Cre;Rosa26-iDTR mice at two different phases of bleomycin-induced lung injury. For early ablation, we co-administered bleomycin with DT and harvested mice at days 7 and 21. To test the effect of ablation after acute injury, we delivered DT 7 days after bleomycin administration. We assessed fibrosis by lung hydroxyproline content and semiquantitative analysis of picrosirius red-staining. We performed bronchoalveolar lavage to determine cell count and differential. We also interrogated genome-wide mRNA expression at day 7 post injury in whole lung RNA. We focused on the following cell populations for the transcriptional profiling experiments: FoxD1-derived+/Coll-GFP– pericytes (Peri), FoxD1-derived+/Coll-GFP+ pericytes (PeriFibro), and FoxD1-derived–/Coll-GFP+ stromal fibroblasts (Fibro).Results: Compared to DT-insensitive littermates where pericyte-like cells were not ablated, DT-sensitive animals exhibited no difference in fibrosis at day 21 both in the early and late pericyte ablation models. However, early ablation of pericytes reduced acute lung inflammation, as indicated by decreased inflammatory cells. Our data confirm a role for pericytes in regulating pulmonary inflammation in early lung injury.

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