Role of CD55 on Leukocytes during Sepsis in Humans

Abstract

The immune system acts as a natural defense against invading microorganisms and bacterial toxins. During sepsis, the complement regulatory protein CD55 seems to play an important pathophysiological role in the innate immune response. This protein is also known as the decay accelerating factor (DAF), which binds to activated C4b or C3b complement fragments on the cell surface and thereby accelerating the decay of both classical and alternative pathway proteins. Aim of this study was to determine changes of the CD55 on leukocytes during clinical sepsis. The CD55 content on leukocytes was determined by flow cytometry. After permission of the local ethics committee, whole blood was obtained from patients in septic shock (n=12) or healthy volunteers (n=10) to measure CD55 surface expression. Furthermore the clinical outcome (30 day survival) was determined. Leukocytes obtained from patients in septic shock showed a significantly enhanced CD55 expression in comparison to healthy volunteers (Lymphocytes: p = 0,162; Monocytes: p = 0,042; Neutrophils: p = 0,026). Remarkably, a difference between survivors and non-survivors of sepsis was observed: CD55 content in neutrophils from patients who survived an observation period of 30d exhibited higher levels of CD55 than patients who succumbed to sepsis. These data suggest that septic conditions upregulate CD55 expression on neutrophils which might represent an early marker for diagnosis of the immune status and for assessment of the prognosis of the sepsis outcome. This work was supported by NIH Grants No. GM-61656, GM-29507 and HL-31963.