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Depletion and Reconstitution of Macrophages in Mice
08:50

Depletion and Reconstitution of Macrophages in Mice

Published on: August 1, 2012

Depletion of pulmonary intravascular macrophages inhibits acute lung inflammation

Baljit Singh1, Jacqueline W Pearce, Lakshman N Gamage

  • 1Department of Veterinary Biomedical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Canada SK S7N 5B4. baljit.singh@usask.ca

American Journal of Physiology. Lung Cellular and Molecular Physiology
|October 21, 2003
PubMed

Insights

Pulmonary intravascular macrophages (PIMs) promote acute lung inflammation by releasing TNF-alpha, which recruits IL-8-containing platelets. Depleting PIMs reduces inflammation in calves, suggesting a similar mechanism may occur in humans.

Area of Science:

  • Veterinary Medicine
  • Immunology
  • Pulmonary Pathology

Background:

  • Pulmonary intravascular macrophages (PIMs) are found in ruminants and horses, species sensitive to acute lung inflammation.
  • Rats and humans may also recruit PIMs under specific conditions, though less commonly.

Purpose of the Study:

  • To investigate the precise contribution of PIMs to acute lung inflammation in a calf model.
  • To understand the role of PIMs in inflammatory cell recruitment and cytokine release during lung infection.

Main Methods:

  • PIMs were identified using Monastral blue tracer and anti-CD68 immunohistology.
  • PIMs were depleted using gadolinium chloride treatment.
  • Levels of IL-8 and TNF-alpha, and histopathological signs of inflammation were assessed post-infection with Mannheimia hemolytica.

Main Results:

  • Gadolinium chloride effectively depleted PIMs within 48 hours.
  • PIM depletion reduced IL-8 and TNF-alpha positive cells and acute lung inflammation.
  • Platelets were identified as the primary IL-8-containing inflammatory cells, releasing IL-8 upon thrombin exposure.

Conclusions:

  • PIMs, as a source of TNF-alpha, promote acute lung inflammation by recruiting IL-8-positive platelets.
  • These findings highlight a novel mechanism of lung inflammation involving PIMs and platelets.
  • The results may be relevant to human lung inflammation due to PIMs' potential recruitment in humans.

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