Neutrophil depletion inhibits early and late monocyte/macrophage increase in lung inflammation

Front Biosci. 2006 May 1:11:1569-76. doi: 10.2741/1904.

Abstract

Monocytes/macrophages have critical impact on outcomes of lung inflammation. Kinetics and mechanisms for the increase of monocytes/macrophages in lungs are not completely understood. To better understand these mechanisms, E. coli-LPS (250 micro grams; N = 35) or endotoxin-free saline (N = 5) were instilled intratracheally in Sprague-Dawley rats and the increase in monocytes/macrophages, neutrophils and monocyte chemotactic protein-1 (MCP-1) was quantified at various time points after LPS treatment. In contrast to typical pattern of neutrophil influx between 6 and 24 hours, monocytes/macrophages increased in two distinct phases, very early at 3 hours and late at 24 hours. The role of neutrophils in monocyte/macrophage increase was addressed in LPS-challenged neutropenic rats (N = 8). Neutrophil depletion before instillation of LPS abrogated the early as well as late monocyte/macrophage increases in the lung. Quantification of MCP-1, which is one of the major chemoattractants for monocytes, in lung homogenates showed similar concentrations in neutropenic and non-neutropenic LPS-challenged rats. These findings show that increase in monocytes/macrophages in lung occurs in two, early and late phases, both being dependent on neutrophils but not on MCP-1.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Chemokine CCL2 / metabolism
  • Escherichia coli / metabolism
  • Immunohistochemistry
  • Inflammation / metabolism*
  • Kinetics
  • Lipopolysaccharides / metabolism
  • Lung / metabolism
  • Lung / pathology*
  • Macrophages / cytology*
  • Macrophages / metabolism
  • Male
  • Microscopy, Electron
  • Microscopy, Immunoelectron
  • Models, Statistical
  • Monocytes / cytology*
  • Monocytes / metabolism
  • Neutropenia
  • Neutrophils / metabolism*
  • Pneumonia*
  • Rats
  • Rats, Sprague-Dawley
  • Time Factors

Substances

  • Chemokine CCL2
  • Lipopolysaccharides