SummarySerum amyloid A (SAA) is an acute phase protein that in the blood is bound to high density lipoproteins; SAA is secreted mainly by hepatocytes, and its concentration increases in the blood up to 1000 times during an inflammatory response. At present, its biological function is unclear. Since some forms of secondary amyloidosis are caused by deposition in tissues of peptides derived from the SAA and leukocytes seem to be involved in this process, we investigated the effect of human SAA on human monocytes and polymorphonuclear cells (PMN). When recombinant human SAA (rSAA) was used at concentrations corresponding to those found during the acute phase (>0.8 /zM), it induced directional migration of monocytes and polymorphonuclear leukocytes. Preincubation of rSAA with high density lipoproteins blocked this chemoattractant activity for both monocytes and PMN. rSAA also regulated the expression of the adhesion proteins CD11b and leukocyte cell adhesion molecule I and induced the adhesion of PMN and monocytes to umbilical cord vein endothelial cell monolayers. When subcutaneously injected into mice, rSAA recruited PMN and monocytes at the injection site. On the basis of these data, we suggest that SAA may participate in enhancing the migration ofmonocytes and PMN to inflamed tissues during an acute phase response.

HE OPPORTUNITY FOR PRIMARY prevention of cardiovascular disease (CVD) begins during childhood. 1 Specifically,earlylesions of atherosclerosis are present in the arteries of children and adolescents 2 ; some children display moderate to high levels of physiologic risk factors 3 ; and childhood levels of physiologic risk factors may predict adult levels. 3-5 Recent studies suggest that plasma homocysteine concentration may be an independent and modifiable risk factor for CVD in adults. 6 A meta-analysis found for every 5-µmol/L increase in homocysteine, the odds ratio for risk of coronary artery disease was 1.6 (95% confidence interval [CI], 1.4-1.7) for men and 1.8 (95% CI, 1.4-2.3) for women. 7 Although conclusive evidence for a causal association with CVD in adults is lacking, 7-17 the potential for prevention provides a strong rationale for understanding the determinants of homocysteine in children.

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