title: The increase of endothelial progenitor cells in the peripheral blood: a new parameter for detecting onset and severity of sepsis.
abstract: Sepsis is a clinical syndrome characterized by non-specific inflammatory response with evidence of profound changes in the function and structure of endothelium. Recent evidence suggests that vascular maintenance, repair and angiogenesis are in part mediated by recruitment from bone marrow (BM) of endothelial progenitor cells (EPCs). In this study we were interested in whether EPCs are increasingly mobilized during sepsis and if this mobilization is associated with sepsis severity. Our flow cytometry data demonstrate that in the CD34+ cell gate the number of EPCs in the blood of patients with sepsis had a four-fold increase (45 +/- 4.5% p < 0.001) compared to healthy controls (12 +/- 3.6%) and that this increase was already evident at 6 hours from diagnosis (40.6 +/- 4.2 percent), reaching its maximum at 72 hours. Also the percentage of cEPCs identified in the patients with sepsis (35 +/- 4.6% of the CD34+ cell) was statistically different (p < 0.001) compared to that found in the blood of patients with severe sepsis (75 +/- 4.9%). In addition, we proved that at six hours after sepsis diagnosis, VEGF, CXCL8 and CXCL12 serum levels were significantly higher in septic patients compared to healthy volunteers 559 +/- 82.14 pg/ml vs 2.9 +/- 0.6 (p < 0.0001), 189.8 +/- 67.3 pg/ml 15 vs 11.9 +/- 1.6 (p = 0.014) and 780.5 +/- 106.5 pg/ml; vs 190.2 +/- 71.4 (p < 0.001). Our data suggest that the cEPC evaluation in peripheral blood, even at early times of diagnosis, in patients with sepsis can be envisaged as a valuable parameter to confirm diagnosis and suggest further prognosis.
authors.affiliation: Department of Medical and Surgical Critical Care, Section of Anaesthesia and Intensive Care, Florence, Italy.
authors.forename: C
authors.initials: C
authors.lastname: Becchi
authors.forename: S
authors.initials: S
authors.lastname: Pillozzi
authors.forename: L P
authors.initials: LP
authors.lastname: Fabbri
authors.forename: M
authors.initials: M
authors.lastname: Al Malyan
authors.forename: C
authors.initials: C
authors.lastname: Cacciapuoti
authors.forename: C
authors.initials: C
authors.lastname: Della Bella
authors.forename: M
authors.initials: M
authors.lastname: Nucera
authors.forename: M
authors.initials: M
authors.lastname: Masselli
authors.forename: S
authors.initials: S
authors.lastname: Boncinelli
authors.forename: A
authors.initials: A
authors.lastname: Arcangeli
authors.forename: A
authors.initials: A
authors.lastname: Amedei
mesh_terms: D000071916:AC133 Antigen; D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD / Q000032:analysis; D018952:Antigens, CD34 / Q000032:analysis; D002452:Cell Count; D054377:Chemokine CXCL12 / Q000097:blood; D042783:Endothelial Cells / Q000166:cytology*; D005434:Flow Cytometry; D006023:Glycoproteins / Q000032:analysis; D006412:Hematopoietic Stem Cells / Q000502:physiology*; D006801:Humans; D016209:Interleukin-8 / Q000097:blood; D008875:Middle Aged; D010455:Peptides / Q000032:analysis; D018805:Sepsis / Q000097:blood*; D042461:Vascular Endothelial Growth Factor A / Q000097:blood
chemical_list: D000071916:AC133 Antigen; D015703:Antigens, CD; D018952:Antigens, CD34; C515255:CXCL12 protein, human; C508606:CXCL8 protein, human; D054377:Chemokine CXCL12; D006023:Glycoproteins; D016209:Interleukin-8; D010455:Peptides; D042461:Vascular Endothelial Growth Factor A