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Platelet-platelet and platelet-leukocyte interactions induced by outer membrane vesicles from N. meningitidis

Mohammad Reza Mirlashari1, Inger Anne Hagberg, Torstein Lyberg

  • 1Research Forum, Ullevaal University Hospital, Oslo, Norway. m.r.mirlashari@ioks.uio.no

Platelets
|March 19, 2002
PubMed
Abstract

Insights

Outer membrane vesicles (OMVs) from meningococcus significantly increase platelet aggregation and binding to leukocytes. Purified lipopolysaccharide (LPS) also promotes aggregation, highlighting their role in sepsis-related microthrombosis.

Area of Science:

  • Immunology
  • Microbiology
  • Hematology

Background:

  • Meningococcal lipopolysaccharide (LPS) is released via outer membrane vesicles (OMVs).
  • OMVs and LPS are key components in bacterial outer membranes and can interact with host cells.

Purpose of the Study:

  • To investigate the effects of meningococcal outer membrane vesicles (OMVs) and purified lipopolysaccharide (LPS) on blood platelet interactions.
  • To compare the effects of OMV-integrated LPS, purified LPS (P-LPS), and E. coli LPS on platelet aggregation and leukocyte binding.

Main Methods:

  • In vitro stimulation of human whole blood and platelet-rich plasma (PRP) with OMVs, P-LPS, and E. coli LPS.
  • Analysis of platelet aggregation, degranulation (CD62P expression), and platelet-leukocyte heteroconjugate formation using flow cytometry.

Main Results:

  • OMVs significantly increased platelet aggregation (2.1-fold), degranulation (1.8-fold), and binding to monocytes (2.6-fold) and granulocytes (2.8-fold).
  • OMVs also markedly increased large CD45-positive cell aggregates (15.7-fold).
  • Purified LPS (meningococcal and E. coli) increased platelet aggregation and heteroconjugate formation but did not affect degranulation or platelet-leukocyte binding in whole blood.

Conclusions:

  • Meningococcal OMVs and purified LPS promote platelet-platelet and platelet-leukocyte aggregation.
  • These interactions are significant in the pathogenesis of microthrombosis and organ dysfunction in meningococcal septicemia.

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