Diminished complement-activating capacity through the classical pathway in sera from type 2 diabetes mellitus

Abstract

Complement-activating capacity through the classical pathway in type 2 diabetes mellitus (T2DM) was examined in the context of free sialic acid as a potential modulator of complement activation. Complement-activating capacity was investigated in an incubation study of heat-aggregated IgG (HAG) and sera from 42 T2DM patients. The study demonstrated diminished in-vitro complement-activating capacity through the classical pathway in T2DM. Various doses of N-acetyl neuraminic acid (NANA) were incubated with normal serum and HAG. Complement activation product levels decreased in a NANA dose-dependent manner. Isoelectrofocusing analysis in a mixture of NANA and purified C3 indicated that C3 changed pI dose-dependently, resulting in the downregulation of complement activation. The serum levels of free sialic acid were determined by fluorometric assay in the 42 T2DM sera samples, and were significantly increased in patients with diminished complement activation. These data indicate that increased serum sialic acid may become a candidate for decreasing complement-activating capacity in T2DM.

• Complement‐activating capacity
• complement activation products
• heat-aggregated IgG (HAG)
• N-acetyl neuraminic acid (NANA)
• sialic acid
• type 2 diabetes mellitus (T2DM)

Declaration of interests

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.