Macrophage Responses to Epithelial Dysfunction Promote Lung Fibrosis in Aging

Abstract

Aim 1 and 2: Using mouse models of lung injury, fibrosis and epithelial dysfunction, we have demonstrated that microenvironment is a key factor driving phenotype of profibrotic alveolar macrophages. We have shown that epithelial dysfunction promotes recruitment of monocyte-derived alveolar macrophages and leads to exaggerated pulmonary fibrosis.

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Document Details

Document Type
Technical Report
Publication Date
Oct 01, 2018
Accession Number
AD1064005

Entities

People

  • Alexander V. Misharin
  • Scott Budinger

Organizations

  • Northwestern University

Tags

DTIC Thesaurus Topics

  • Biology
  • Biomedical Research
  • Bone Marrow
  • Cells
  • Chemistry
  • Computational Biology
  • Demographic Cohorts
  • Department Of Defense
  • Dysfunction
  • Epithelial Cells
  • Genes
  • Lung Diseases
  • Macrophages
  • Medical Personnel
  • Monocytes
  • Systems Biology
  • Wounds And Injuries

Fields of Study

  • Biology
  • Chemistry
  • Medicine

Readers

  • Immunology and Pathology