ABSTRACT
Serum amyloid A (SAA) is an acute phase reactant that can become the predominant apolipoprotein of high density lipoprotein (HDL) during severe inflammatory states. However, the function of SAA is unknown. To study the ability of SAA to form HDL in the absence of apolipoprotein A-I, we expressed the mouse SAA pI 6.15 (CE/J) isoform in apolipoprotein A-I knock-out (apoA-I (-/-)) mice using a recombinant adenovirus. As a control, apoA-I (-/-) mice were injected with an adenovirus expressing human apoA-I. High level expression of plasma SAA was obtained in the absence of any endogenous acute phase SAA production. SAA expression increased plasma HDL cholesterol levels about 2-fold, but to a lesser extent than the expression of apoA-I (about 10-fold). The HDL particles isolated by density ultracentrifugation from SAA-expressing mice were heterogeneous in size and composition and rich in free cholesterol as well as apoE and apoA-IV. Of the SAA expressed in the plasma, only a small fraction (4%) was associated with HDL particles in contrast to expressed apoA-I, of which 62% was associated with HDL. We conclude that SAA is unable to substitute for apoA-I in HDL particle formation.
Subject(s)
Apolipoprotein A-I/deficiency , Apolipoproteins/genetics , Serum Amyloid A Protein/genetics , Acute-Phase Reaction/blood , Adenoviridae/genetics , Animals , Apolipoprotein A-I/genetics , Apolipoproteins/metabolism , Apolipoproteins A/blood , Apolipoproteins E/blood , Cholesterol/blood , Cholesterol, HDL/blood , Cholesterol, HDL/chemistry , Gene Expression , Genetic Vectors , Humans , Mice , Mice, Inbred C57BL , Mice, Knockout , Serum Amyloid A Protein/metabolismABSTRACT
A search for records for CMV infection following transfusion related to noncardiac and nontransplant operations and trauma disclosed nine instances with CMV seroconversion. One patient had received only a single unit of blood. The most prominent feature was fever with a characteristic spiking plateau pattern, which began approximately three weeks after blood transfusion. Splenomegaly and atypical lymphocytosis were less common. The results of hepatic function tests showed slight abnormalities. Associated splenectomy did not result in a more severe manifestation of the CMV infection. The late postoperative fever in these patients led to an extensive and costly investigation before determination of antibody titers to CMV and confirmation of seroconversion. When faced with the constellation of symptoms, including a delayed (two to three weeks) spiking plateau postoperative fever, abnormal results of hepatic function test and lymphocytosis in patients having received blood transfusion, the clinician must give serious consideration to the possibility of CMV infection.