The acute phase response in Syrian hamsters elevates apolipoprotein serum amyloid A (apoSAA) and disrupts lipoprotein metabolism

Lipoprotein metabolism was assessed in hamsters following subcutaneous injection of AgNO3. Apolipoprotein serum amyloid A (apoSAA) peaked at 36 h, followed by elevations in plasma cholesterol at 56 h and triglycerides at 96 h. There was a striking increase in LDL and a decrease in HDL. Migration of all acute phase (AP) lipoproteins was retarded compared to controls and SDS-PAGE electrophoretic analysis was consistent with agarose gel profiles that revealed increased apoB-rich VLDL, IDL and LDL and decreased apoAI-rich HDL(2) fractions. Cholesterol transported by LDL of AgNO3 treated hamsters was double that of controls while the pool of HDL-cholesterol was only two-thirds that of controls. Fasting triglyceride and cholesterol secretion rates were depressed sharply at 24 h. After E. coli lipopolysaccharide (LPS) injection, apoSAA-HDL particles bound avidly to cultured peritoneal macrophages (m phi s) but in vitro exposure of tissue m phi s to LPS did not alter the binding characteristics of either control- or apoSAA-HDL, Finally, I-125- radiolabelled apoSAA-HDL and apoAI-HDL decreased during 2-4 h exposure to m phi s bur only apoAI remained associated with cells. Collectively, these data support the hypothesis that apoSAA may commandeer HDL during the AP response in order to deliver phospholipids and cholesterol to cells involved in tissue repair at sites of inflammation.