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An aging bone marrow exacerbates lung fibrosis by fueling profibrotic macrophage persistence

Asma Farhat1,2, Mariem Radhouani1,2, Florian Deckert1,2

  • 1Research Division of Infection Biology, Department of Medicine I, Medical University of Vienna, Vienna, Austria.

Science Immunology
|March 28, 2025
PubMed

Insights

Aging bone marrow worsens lung fibrosis by promoting profibrotic macrophages. Regulatory T cells (Tregs) producing IL-10 can restore macrophage balance and aid repair.

Area of Science:

  • Immunology
  • Aging Research
  • Pulmonary Medicine

Background:

  • Pulmonary fibrosis is an age-related incurable disease.
  • The role of hematopoietic aging in lung fibrosis and immune response is not well understood.

Purpose of the Study:

  • To investigate how hematopoietic aging impacts lung immune responses and fibrosis progression.
  • To identify mechanisms by which aged bone marrow exacerbates lung fibrosis.

Main Methods:

  • Utilized heterochronic bone marrow transplant mouse models.
  • Analyzed immune cell accumulation and phenotype in lung tissue post-injury.
  • Assessed the role of interleukin-10 (IL-10) and regulatory T cells (Tregs) in modulating macrophage function.

Main Results:

  • Aged bone marrow exacerbated lung fibrosis, independent of lung tissue age.
  • Cell-intrinsic hematopoietic aging led to increased accumulation of profibrotic monocyte-derived alveolar macrophages (Mo-AMs).
  • Reduced pulmonary IL-10 and impaired Mo-AM maturation were observed, driven by extrinsic environmental signals.
  • Regulatory T cells (Tregs) were identified as key IL-10 producers that promote Mo-AM maturation and reduce fibrosis.

Conclusions:

  • Hematopoietic aging significantly impacts lung immune regulation and fibrosis.
  • Treg-mediated IL-10 signaling is crucial for Mo-AM maturation and attenuating lung fibrosis.
  • Targeting Treg-IL-10 pathways offers a potential therapeutic strategy for pulmonary fibrosis and promoting tissue repair.

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