Blood Journal
Leading the way in experimental and clinical research in hematology

Antibacterial effect of microvesicles released from human neutrophilic granulocytes

  1. Csaba I. Timár1,
  2. Ákos M. Lorincz1,
  3. Roland Csépányi-Kömi1,
  4. Anna Vályi-Nagy1,
  5. György Nagy2,
  6. Edit I. Buzás2,
  7. Zsolt Iványi3,
  8. Ágnes Kittel4,
  9. David W. Powell5,
  10. Kenneth R. McLeish6, and
  11. Erzsébet Ligeti1,*
  1. 1 Department of Physiology, Semmelweis University, Budapest, Hungary;
  2. 2 Department of Genetics, Cell Biology and Immunobiology of Semmelweis University, Budapest, Hungary;
  3. 3 Clinic for Anaesthesiology and Intensive Care of Semmelweis University, Budapest, Hungary;
  4. 4 Institute of Experimental Medicine of the Hungarian Academy of Sciences, Budapest, Hungary;
  5. 5 Departments of Medicine and of Biochemistry and Molecular Biology, University of Louisville, Louisville, KY, United States;
  6. 6 Robley Rex VA Medical Center, Louisville, KY, Hungary
  1. * Corresponding author; email: ligeti{at}


Cell-derived vesicles represent a recently discovered mechanism for intercellular communication. In the present study we investigated their potential role in interaction of microbes with host organisms. We provide evidence that different stimuli induced isolated neutrophilic granulocytes to release microvesicles with different biological properties. Only opsonized particles initiated the formation of microvesicles that were able to impair bacterial growth. The antibacterial effect of neutrophil-derived microvesicles was independent of production of toxic oxygen metabolites and opsonization or engulfment of the microbes, but depended on β2 integrin function, continuous actin remodeling and on the glucose supply. Neutrophil-derived microvesicles were detected in the serum of healthy donors, and their number was significantly increased in the serum of bacteremic patients. We propose a new extracellular mechanism to restrict bacterial growth and dissemination.

  • Submitted May 24, 2012.
  • Accepted October 18, 2012.