Experimental polymyxin B-induced interstitial lung disease characterized by an accumulation of cytotoxic eosinophils in the alveolar structures. Academic Article uri icon

Overview

MeSH

  • Aerosols
  • Animals
  • Disease Models, Animal
  • Female
  • Guinea Pigs
  • Lung
  • Polymyxin B
  • Reference Values

MeSH Major

  • Eosinophils
  • Pulmonary Alveoli
  • Pulmonary Fibrosis

abstract

  • A variety of lung disorders are associated with the accumulation of eosinophils in the alveolar structures. To help understand the role of eosinophils in these disorders, an animal model of eosinophilic lung disease was developed. Administration of an aerosol of polymyxin B to guinea pigs (3 times per wk for 4 wk) produced diffuse interstitial lung disease with alveolar wall thickening and an alveolitis characterized by marked increases in eosinophils and alveolar macrophages. Bronchoalveolar lavage confirmed the presence of significantly increased numbers of eosinophils and alveolar macrophages in polymyxin-B-treated animals compared with those in control animals. Using density gradient centrifugation, approximately 10(7) eosinophils could be purified from the lungs of a single polymyxin-B-treated animal. Importantly, eosinophils purified from the lungs from polymyxin B-treated animals exhibited significant spontaneous cellular cytotoxicity for human fetal lung fibroblasts. In contrast, neither eosinophils from control animals nor alveolar macrophages from either group of animals were cytotoxic. These findings demonstrate that eosinophils possess effector processes capable of injuring the lung parenchyma and suggest that eosinophils can contribute to the pathogenesis of the interstitial lung disease.

publication date

  • January 1985

has subject area

  • Aerosols
  • Animals
  • Disease Models, Animal
  • Eosinophils
  • Female
  • Guinea Pigs
  • Lung
  • Polymyxin B
  • Pulmonary Alveoli
  • Pulmonary Fibrosis
  • Reference Values

Research

keywords

  • Journal Article

Identity

Language

  • eng

PubMed ID

  • 3966696

Additional Document Info

start page

  • 103

end page

  • 108

volume

  • 131

number

  • 1