Activation of the Properdin Pathway of Complement in Patients with Gram-Negative Bacteremia

TLDR

Biologically active products released during activation of C3‑C9 may contribute to the development of shock. The study aimed to identify the complement activation pathway in gram‑negative bacteremia by measuring serum levels of C1, C4, C2, C3, C5, C6, C9, properdin, and factor B in 42 patients, including 19 who later developed shock. Serum concentrations of complement components and properdin factors were quantified in 42 gram‑negative bacteremia patients, with 19 subsequently developing shock. Patients who developed shock had significantly lower levels of properdin, factor B, and C3, C5, C6, and C9, while classical components C1, C4, and C2 were unchanged, indicating that C3 and the terminal complement cascade are primarily activated via the properdin pathway in shock‑associated gram‑negative bacteremia.

Abstract

To determine the pathway used for activation of complement component C3, serum levels of components C1, C4, C2, C3, C5, C6, and C9 and two properdin factors, properdin and factor B, were measured in 42 patients with gram-negative bacteremia, in 19 of whom shock subsequently developed. Mean levels of the classical components C1, C4, and C2 in bacteremic patients in whom shock subsequently developed did not differ significantly (p greater than 0.05) from those of patients with uncomplicated bacteremia. Levels of properdin, factor B and C3, C5, C6, and C9 were significantly (p less than 0.05) decreased in patients with shock in comparison with those with uncomplicated bacteremia. Taken together, these findings are consistent with activation of C3 and the terminal complement sequence, C5-C9, occurring primarily by the properdin pathway, in patients with gram-negative bacteremia eventuating in shock. Biologically active products released during activation of C3-C9 may contribute to the development of shock.