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Effect of E. coli outer membrane vesicles on monocyte‐platelet aggregates (145.9)
Author(s) -
Dobrydneva Yuliya,
Wahab Kamal,
Soult Michael,
Lonergan Natalie,
Sullivan Claretta
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.145.9
Subject(s) - platelet , incubation , flow cytometry , whole blood , bacterial outer membrane , vesicle , monocyte , chemistry , sepsis , cd14 , endothelium , andrology , microbiology and biotechnology , immunology , biology , membrane , medicine , biochemistry , endocrinology , escherichia coli , gene
Bacterial outer membrane vesicles (OMVs) can initiate the inflammatory response in the transition of an infection to sepsis, and sepsis is a prothrombotic state. The role of OMVs in the development of prothrombotic tendency is unknown. The objective: to determine whether OMVs and endothelial microparticles can induce formation of prothrombotic monocyte‐platelet aggregates (MPA). Donor blood was incubated either with OMVs from clinical isolate of an enterotoxigenic strain of E. coli or with supernatant from HUVEC (Human Umbilical Endothelial Cells) cultured in the presence of OMV for 24 hrs. MPA were measured in whole blood by flow cytometry as CD61+CD14+ cells. In whole blood from healthy human volunteers, MPA level is 19±2% in unstimulated state and 37±8% in ADP‐stimulated state. Incubation of blood with OMVs did not significantly increase MPA neither in unstimulated blood (23±2%), nor in ADP‐stimulated blood (24±7%). However, supernatant from HUVEC cultured with OMVs increased level of MPA in ADP‐stimulated blood (54±9%). Incubation with microparticles‐free HUVEC supernatant decreases MPA in ADP‐stimulated blood to a control level (35±4%). Thus, it is likely that microparticles derived from OMV‐treated HUVEC increase MPA. Therefore OMV may contribute to a prothrombotic state by stimulating microparticles release from activated endothelium and increasing prothrombotic MPA formation.