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This article is available online at http://www.jlr.org herpes simplex virus, helicobacter pylori, as well as periodontitis have been studied ( 2-4 ). On the contrary, other studies have disputed the causal role of infectious agents in atherogenesis ( 5-7 ).Current evidence suggests that atherosclerosis develops as a response to infl ammatory stimulus. Therefore, common or uncommon infections could represent a risk factor. Mechanisms that may be implicated in the atherogenesis caused by infectious agents include local increase of proinfl ammatory cells, local effusion of endotoxins, autoimmune reaction, systemic cytokine release, and changes in lipid metabolism ( 8 ).Infection and infl ammation cause similar cytokineinduced changes in lipid and lipoprotein metabolism ( 9 ). These include reductions in serum levels of total cholesterol (TC), HDL-cholesterol (HDL-C), LDL-cholesterol (LDL-C), apolipoproteins (Apo) AI and B, and lipoprotein (a) [Lp(a)] and increases in triglyceride (TG) and ApoE concentrations ( 9-14 ).Current evidence suggests that the host response to infection and infl ammation increases oxidized lipids in serum and induces LDL oxidation in vivo. Oxidative modifi cation of LDL is an important event in the development of atherosclerosis ( 15 ). In addition, the cholesterol ester transfer protein (CETP) plays a central role in HDL metabolism and the regulation of HDL-C levels in serum. High levels of CETP activity lead to a reduction in HDL-C levels and an atherogenic lipoprotein profi le ( 16 ).Platelet-activating factor (PAF) is a potent pro-infl ammatory phospholipid produced by activated platelets, -C), ApoB, ApoAI, and ApoCIII and higher LDL-C/HDL-C and ApoB/ApoAI ratios; 2 ) higher levels of IL-1b, IL-6, and TNFa; 3 ) similar ApoCII and oxLDL levels and Lp-PLA 2 activity, lower PON1, and higher CETP activity; and 4 ) higher small dense LDL-C concentration. Four months later, increases in TC, HDL-C, LDL-C, ApoB, ApoAI, and ApoCIII levels, ApoB/ApoAI ratio, and PON1 activity were noticed compared with baseline, whereas CETP activity decreased. LDL-C/HDL-C ratio, ApoCII, and oxLDL levels, Lp-PLA 2 activity, and small dense LDL-C concentration were not altered. Brucella infection is associated with an atherogenic lipid profi le that is not fully restored 4 months following treatment. There is increasing evidence that a link exists between infection/infl ammation and atherosclerosis ( 1 ). Infections with chlamydia pneumoniae, cytomegalovirus,

The objective of the present study was to evaluate the effects of acute infection with Leptospira interrogans on lipids, lipoproteins and associated enzymes. Fasting serum levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), apolipoproteins (apo) A-Ι, B, E, C-II, C-III and lipoprotein (a) [Lp(a)] were determined in patients with Leptospirosis on diagnosis and 4 months after recovery as well as in age- and sex-matched controls. Activities of cholesteryl-ester transfer protein (CETP) and lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) as well as paraoxonase 1 (PON1) hydrolysing activity and levels of cytokines were determined. LDL subclass analysis was performed with Lipoprint LDL System. Eleven patients (10 men, mean age 49.5 ± 8.4 years) and 11 controls were included. TC, HDL-C, LDL-C, apoA-I, apoB and Lp(a) levels were lower at baseline, whereas TG and apoE levels were elevated compared with 4 months later. At baseline, higher levels of cytokines and cholesterol concentration of small dense LDL particles (sdLDL-C) were noticed, whereas LDL particle size was lower compared with follow-up. Activities of plasma Lp-PLA(2) and HDL-associated Lp-PLA(2) were lower at baseline compared with post treatment values, whereas PON1 activity was similar at baseline and 4 months later. 4 months after recovery, the levels of all lipid parameters evaluated did not differ compared with controls, except for HDL-C which remained lower. PON1 activity both at baseline and 4 months later was lower in patients compared with controls. Leptospirosis is associated with atherogenic changes of lipids, lipoproteins and associated enzymes.

Visceral leishmaniasis (VL) is a vector-borne protozoal infection caused by replication of Leishmania species in macrophages. VL is characterized by fever, hepatosplenomegaly and cytopenia. Apart from those classic clinical characteristics, VL has been associated with autoimmune clinical and laboratory features. Reported herein are 16 consecutive patients with VL who were checked for laboratory autoimmune manifestations. A variety of autoimmune antibodies including elevated titers of antinuclear antibodies and rheumatoid factor were detected in all patients. Of note, no laboratory autoimmune manifestations were detected in the seven patients who were re-evaluated 3 months after therapy. It is concluded that autoimmune laboratory manifestations during VL infection are common. These may mistakenly lead to diagnosis of an autoimmune disorder.

Patients with VL exhibit increased TG levels and decreased cholesterol subclasses at diagnosis. HDL-C, apoA-I and associated enzymes remain lower 4 months after VL resolution compared with controls.