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Related Experiment Videos

P-selectin mediates intestinal ischemic injury by enhancing complement deposition

S A Gibbs1, M R Weiser, L Kobzik

  • 1Department of Surgery, Brigham and Women's Hospital, Boston, MA 02115, USA.

Surgery
|June 1, 1996
PubMed
Summary

P-selectin antagonism in rodent intestine ischemia reperfusion injury did not reduce neutrophil sequestration but did inhibit complement deposition. This suggests a novel protective mechanism beyond neutrophil adhesion.

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Area of Science:

  • Gastroenterology
  • Immunology
  • Vascular Biology

Background:

  • Intestinal ischemia and reperfusion injury in rodents is mediated by the complement system.
  • P-selectin antagonism shows promise in reducing local injury, but its mechanism remains unclear as neutrophil depletion does not confer protection.

Purpose of the Study:

  • To investigate whether P-selectin antagonists protect against intestinal ischemia and reperfusion injury by inhibiting complement activation.
  • To elucidate the role of P-selectin antagonism in modulating neutrophil sequestration and complement deposition during intestinal injury.

Main Methods:

  • Rodents (n=86) underwent 50 minutes of mesenteric ischemia followed by 4 hours of reperfusion.
  • Treatment groups included a monoclonal antibody against P-selectin (PB1.3), soluble sialyl Lewisx (sLex), saline control, and sham.

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  • Intestinal injury was assessed by 125I-albumin permeability and myeloperoxidase (MPO) assay; complement deposition (C5b-9) and neutrophil sequestration were evaluated via immunohistochemistry and MPO assays.

    • Main Results:

    • PB1.3 treatment significantly reduced intestinal 125I-albumin permeability compared to saline controls (p < 0.05) but did not alter neutrophil sequestration.
    • PB1.3 significantly reduced mucosal C5b-9 deposition, indicating complement inhibition.
    • sLex reduced intestinal MPO activity (p < 0.05) but not permeability, while both PB1.3 and sLex showed effects on remote lung injury markers.

    Conclusions:

    • P-selectin antagonism, specifically targeting the lectin domain, does not confer local benefit by inhibiting neutrophil adhesion in this model.
    • PB1.3 demonstrates a novel protective mechanism by antagonizing P-selectin and reducing complement deposition in the intestinal mucosa.
    • The findings suggest that complement inhibition, rather than direct neutrophil adhesion blockade, may be the primary protective pathway for P-selectin antagonists in this context.