Chlamydia pneumoniae antibodies and serum lipids in Finnish men: cross sectional study

Introduction

Chlamydia pneumoniae is an intracellular Gram negative bacterium that commonly causes respiratory infections. C pneumoniae infection has been associated with atherosclerosis in seroepidemiological studies, and the organism was recently found within atherosclerotic lesions.1 It is also known that acute infections interfere with lipid metabolism. Raised concentrations of triglycerides have been detected in Gram negative infections, and concentrations of high density lipoprotein cholesterol have been shown to decrease in both bacterial and viral infections.2 We studied the effect of C pneumoniae infection on serum lipid concentrations.

Methods and results

The study population consisted of 1053 men who participated in a reindeer herders' health survey performed in Finland 1986-9.3 Blood samples were taken after 12 hours of fasting. Total cholesterol, high density lipoprotein cholesterol, and triglyceride concentrations were measured by routine enzymatic methods. Serum IgG and IgA antibodies specific for C pneumoniae antibodies were determined by the microimmunofluorescence method using C pneumoniae strain Kajaani 6 as an antigen. Analysis of covariance with age as a covariate was used to test concentrations of serum triglyceride, total cholesterol, and high density lipoprotein and ratios of high density lipoprotein cholesterol to total cholesterol in groups classified by smoking and antibodies specific to C pneumoniae.

The mean age of the study group was 47 (range 20 to 87) years; 32% (337) were current smokers. Both antibody prevalence and the age adjusted geometric mean antibody titres were significantly higher in smokers than in non-smokers; IgG antibodies were present (titre ≥32) in 83% (280/337) of smokers and in 77% (417/542) of non-smokers (P<0.01). Overall the geometric mean triglyceride concentration was 1.14 (range 0.32-9.07) mmol/l, the mean total cholesterol concentration 6.4 (3.1-11.2) mmol/l, and the mean high density lipoprotein cholesterol concentration 1.26 (0.56-3.11) mmol/l. The geometric mean ratio of high density lipoprotein cholesterol to total cholesterol was 0.19 (0.07-0.72). Triglyceride and total cholesterol concentrations were higher and high density lipoprotein cholesterol concentrations lower in smokers than in non-smokers. Table 1) shows age adjusted geometric means and ratios according to C pneumoniae specific IgG antibody titres and smoking. In non-smokers, triglyceride concentrations increased and high density lipoprotein cholesterol concentrations and high density lipoprotein cholesterol:total cholesterol ratios decreased significantly (P=0.017, 0.001, and 0.001, respectively) according to IgG antibody titres; values did not differ significantly in smokers. Overall, subjects positive for IgG had significantly higher triglyceride concentrations and lower high density lipoprotein cholesterol concentration and the high density lipoprotein cholesterol:total cholesterol ratios (P=0.06, 0.003, and 0.007, respectively). Presence of IgA antibodies (titre ≥16) had only a minor association with lipid concentrations.

Comment

Changes in lipid metabolism are well recognised in the pathogenesis of atherosclerosis. High concentrations of triglycerides and low concentrations of high density lipoprotein cholesterol, as well as low ratios of high density lipoprotein cholesterol:total cholesterol, are known to be important risk factors for coronary heart disease.

The specific IgG antibodies in these men suggest that they have been infected by C pneumoniae or have a persistent C pneumoniae infection; the altered serum lipid values may thus reflect disturbances in lipid metabolism caused by infection. As a Gram negative bacterium, C pneumoniae contains lipopolysaccharide as a major constituent of its outer membrane. It can multiply in macrophages, smooth muscle, and endothelial cells and induce production of tumor necrosis factor and interleukin-1.1 In macrophages and smooth muscle cells in atherosclerotic lesions C pneumoniae and its lipopolysaccharide may lead to continuous production of cytokines and thus to an altered serum lipid profile. Several other chronic bacterial infections such as Helicobacter pylori infection have recently been connected to atherosclerosis.4 If these infections contribute even partly to the altered serum lipid profile, eradication of the infection by antibiotic treatment would decrease the risk of atherosclerotic disease.