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Related Experiment Video

Updated: Jul 29, 2025

Flow Cytometric Isolation of Primary Murine Type II Alveolar Epithelial Cells for Functional and Molecular Studies
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Interleukin-11 disrupts alveolar epithelial progenitor function.

Rosa K Kortekaas1,2, Kerstin E Geillinger-Kästle3, Theo Borghuis4

  • 1Department of Molecular Pharmacology, University of Groningen, Groningen, the Netherlands.

ERJ Open Research
|May 25, 2023
PubMed
Summary

Interleukin-11 (IL-11) disrupts lung repair by impairing alveolar epithelial regeneration. This study shows IL-11 inhibits progenitor cell activation, hindering the development of mature alveolar cells in idiopathic pulmonary fibrosis.

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Area of Science:

  • Pulmonary Medicine
  • Cell Biology
  • Fibrosis Research

Background:

  • Interleukin-11 (IL-11) is implicated in idiopathic pulmonary fibrosis (IPF) pathogenesis.
  • IL-11 promotes myofibroblast differentiation and collagen deposition.
  • The impact of IL-11 on dysregulated alveolar repair in IPF is not fully understood.

Purpose of the Study:

  • To investigate the role of IL-11 in alveolar epithelial repair.
  • To determine if IL-11 disrupts epithelial-fibroblast communication during lung repair.
  • To analyze the distribution of IL-11 and its receptor (IL-11R) in human IPF lungs.

Main Methods:

  • Utilized mouse lung organoids and precision-cut lung slices (PCLS) to study IL-11 effects on alveolar repair.
  • Employed immunohistochemistry to assess IL-11 and IL-11R distribution in human lung tissues.
  • Performed bulk RNA-sequencing on human fibroblasts treated with IL-11.

Main Results:

  • IL-11 was detected in airway epithelium, macrophages, and hyperplastic AT2 cells in IPF lungs.
  • IL-11 reduced organoid formation and Prosurfactant Protein C expression in epithelial progenitor cultures, indicating impaired regeneration.
  • IL-11 increased ciliated cell markers in PCLS and modulated key IPF-associated pathways in human fibroblasts.

Conclusions:

  • IL-11 disrupts alveolar epithelial regeneration by inhibiting progenitor activation and mature cell formation.
  • The study provides limited evidence for a significant role of dysregulated fibroblast-epithelial communication in this process.
  • IL-11 emerges as a key mediator of impaired lung repair in IPF.