Elastin fragments attract macrophage precursors to diseased sites in pulmonary emphysema. Academic Article uri icon

Overview

MeSH

  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Humans
  • Macrophages
  • Peptide Fragments
  • Structure-Activity Relationship

MeSH Major

  • Chemotaxis, Leukocyte
  • Elastin
  • Monocytes
  • Pulmonary Emphysema
  • Tropoelastin

abstract

  • This study suggests one mechanism by which alveolar macrophages accumulate in the lung in pulmonary emphysema: elastin fragments generated at the diseased sites are potent chemoattractants for monocytes, the precursors of the macrophages. The most chemotactic elastin fragments have a molecular weight between 10,000 and 50,000 and are active at concentrations as low as 3 nanograms per milliliter. By comparison, elastin fragments with higher molecular weights and desmosines are active at concentrations greater than 0.3 microgram per milliliter. In addition, preincubation of monocytes with the 10,000- to 50,000-dalton elastin impairs the ability of the cells to migrate toward elastin fragments but not toward activated serum. Fragments of tropoelastin are not chemotactic for monocytes. Because elastin, but not tropoelastin, contains lysyl-derived cross-links, these structures may be the active chemotactic site on the elastin fragments.

publication date

  • May 22, 1981

has subject area

  • Cells, Cultured
  • Chemotaxis, Leukocyte
  • Dose-Response Relationship, Drug
  • Elastin
  • Humans
  • Macrophages
  • Monocytes
  • Peptide Fragments
  • Pulmonary Emphysema
  • Structure-Activity Relationship
  • Tropoelastin

Research

keywords

  • Journal Article

Identity

Language

  • eng

PubMed ID

  • 7233186

Additional Document Info

start page

  • 925

end page

  • 927

volume

  • 212

number

  • 4497