CD64 upregulation on peripheral granulocytes is not a marker of sepsis and does not correlate with serum concentrations of granulocyte colony-stimulating factor (G-CSF) in postoperative/posttraumatic patients with severe sepsis
© Current Science Ltd 1998
Published: 1 March 1998
To study whether the modulation of the expression of CD64 on the surface of neutrophils correlates with the inflammatory response and changes in serum concentrations of G-CSF in postoperative/posttraumatic patients with severe sepsis and septic shock.
Sixteen of these patients were studied upon admission to the intensive care unit (ICU) staying for more than 5 days. In these patients, a longitudinal analysis on the kinetics of leukocyte counts, the expression of CD64 and G-CSF serum concentrations was performed on a daily basis until discharge from the ICU. Surface expression was tested by flow cytometry using a Coulter Epics XL-MCL (Coulter Electronis, Krefeld, Germany). Results are expressed as a ratio between the mean channel value of the CD64-positive granulocyte fraction and the isotype control IgG1, ie CD64/IgG1.
In all patients, CD64 was homogeneously expressed on all granulocytes. Six out of the 16 patients responded with an increase in CD64/IgG1 > 2.5 following manifestation of an infectious focus. In the remaining 10 patients CD64/IgG1 remained or declined below 2.5 and even below 1.5 despite bacterial infection, severe sepsis and septic shock. High expression of CD64-density (ratio > 2.5) occured incidentally with low serum concentrations of G-CSF (< 170 pg/ml) in individual patients and vice versa, i. e., low CD64 ratio < 1.5 and high G-CSF (up to 65,000 pg/ml). In a single patient with shock not due to infection, CD64/IgG1 remained below 1.7, despite serum concentrations of G-CSF up to 2300 pg/ml. Serum concentrations of G-CSF did not correlate with the expression of CD64 (r = 0.02–0.61 for individual patients).
G-CSF has been proven a relevant hematopoietic factor to cope with acute inflammation and sepsis in vivo. CD64 expression has been suggested to indicate G-CSF serum activity and activation of neutrophils in vivo, and to serve as a marker of sepsis. The non-responsiveness of CD64 to G-CSF indicates that other factors must be involved and that active counterregulatory effects occur in patients with severe sepsis and septic shock. Thus, CD64 expression cannot serve as a longterm marker of sepsis.