Association of Chlamydia pneumoniae with coronary artery disease and its progression is dependent on the modifying effect of mannose-binding lectin.
BACKGROUND
The possible association between coronary artery disease (CAD) and Chlamydia pneumoniae (C pneumoniae) infection is controversial. On the basis of the recent suggestion that mannose-binding lectin (MBL) variant alleles are related to an increased risk of severe atherosclerosis, and on the in vitro interaction of MBL with C pneumoniae, we asked whether MBL might contribute to CAD in conjunction with C pneumoniae.


RESULTS
Antibodies to C pneumoniae were measured by immunofluorescence and MBL alleles were determined by polymerase chain reaction technique in samples from 210 patients with CAD and 257 healthy subjects from Hungary collected between 1995 and 1996. A higher percentage of patients with CAD were anti-C pneumoniae positive as compared with the control group (P=0.058). However, at logistic regression analysis adjusted to age, sex, and serum lipid levels, this difference was confined only to subjects carrying MBL variant alleles (P=0.035, odds ratio 2.63, [95% CI: 1.07 to 6.45]). In contrast, no significant difference was seen in those homozygous for the normal MBL allele (P=0.412). During a 65+/-5.8-month follow-up period, major outcomes (new myocardial infarction, and/or bypass operation or cardiovascular death) occurred in 11 C pneumoniae positive and 3 C pneumoniae negative patients. In the C pneumoniae positive group, the odds ratio of development of outcomes was 3.27 (95% CI: 1.10 to 9.71, P=0.033) in the carriers of the MBL variant alleles compared with the homozygous carriers of the normal MBL allele.


CONCLUSIONS
These results indicate that infection with C pneumoniae leads mainly to the development and progression of severe CAD in patients with variation in the MBL gene.
Rugonfalvi-Kiss
Szabolcs
S
3rd Department of Medicine, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Endrész
Valéria
V
Madsen
Hans O
HO
Burián
Katalin
K
Duba
Jenô
J
Prohászka
Zoltán
Z
Karádi
István
I
Romics
László
L
Gönczöl
Eva
E
Füst
George
G
Garred
Peter
P
D000483:Alleles; D000907:Antibodies, Bacterial / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D002352:Carrier Proteins / Q000235:genetics*; D018834:Chaperonin 60 / Q000276:immunology; D023521:Chlamydophila Infections / Q000097:blood / Q000453:epidemiology* / Q000276:immunology; D016993:Chlamydophila pneumoniae / Q000276:immunology; D037222:Collectins; D015897:Comorbidity; D003324:Coronary Artery Disease / Q000097:blood / Q000453:epidemiology* / Q000276:immunology; D003710:Demography; D018450:Disease Progression; D005260:Female; D005787:Gene Frequency; D006580:Genetic Carrier Screening; D014644:Genetic Variation; D006801:Humans; D006814:Hungary / Q000453:epidemiology; D007074:Immunoglobulin G / Q000097:blood; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D011110:Polymorphism, Genetic; D011237:Predictive Value of Tests; D012307:Risk Factors; D016036:Seroepidemiologic Studies
D000907:Antibodies, Bacterial; D002352:Carrier Proteins; D018834:Chaperonin 60; D037222:Collectins; D007074:Immunoglobulin G; D002097:C-Reactive Protein