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Related Experiment Videos

PMNs primed for superoxide release and increased CD11b expression do not sequester in normal lung

B Fontes1, E E Moore, F A Moore

  • 1Department of Surgery, Denver General Hospital, Colorado 80204-45007, USA.

The Journal of Surgical Research
|June 1, 1995
PubMed
Summary

Platelet activating factor (PAF) primes neutrophils, but this priming alone does not cause lung sequestration. Additional factors from gut ischemia/reperfusion injury are required for neutrophil accumulation in the lungs.

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Area of Science:

  • Physiology
  • Immunology
  • Pathology

Background:

  • Previous research linked platelet activating factor (PAF)-induced neutrophil (PMN) priming and CD11b/CD18 expression to lung injury after gut ischemia/reperfusion (I/R).
  • CD11b blockade reduced lung injury but did not affect PMN priming or pulmonary leukosequestration in this model.

Purpose of the Study:

  • To test the hypothesis that PAF-stimulated PMN priming and CD11b expression are insufficient to cause lung PMN sequestration.
  • To investigate the role of gut I/R-generated factors in PMN sequestration.

Main Methods:

  • Normal rat PMNs were labeled with 51Cr and primed with PAF to enhance superoxide generation and CD11b expression.
  • Gut I/R was induced in rats via superior mesenteric artery occlusion.
  • 51Cr-labeled PMNs (normal or PAF-primed) were administered to control, sham, or gut I/R rats.

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Main Results:

  • PAF-primed PMNs exhibited increased superoxide release and CD11b expression.
  • PAF-primed PMNs did not sequester in the lungs of normal rats.
  • Following gut I/R, PAF-primed PMNs sequestered significantly in the pulmonary vasculature.

Conclusions:

  • PAF priming of neutrophils, including enhanced superoxide generation and CD11b expression, is insufficient on its own to promote PMN sequestration in the lungs.
  • Additional factors produced during gut I/R are necessary to facilitate PMN sequestration in the pulmonary bed.