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Clinical and Vaccine Immunology, January 2008, p. 55-59, Vol. 15, No. 1
1071-412X/08/$08.00+0     doi:10.1128/CVI.00163-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Association of Chlamydia pneumoniae Infection with HLA-B*35 in Patients with Coronary Artery Disease{triangledown}

Anil Palikhe,1,2 Marja-Liisa Lokki,2 Pekka Saikku,3 Maija Leinonen,4 Mika Paldanius,4 Mikko Seppänen,5 Ville Valtonen,5 Markku S. Nieminen,1 and Juha Sinisalo1*

Division of Cardiology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland,1 Transplantation Laboratory, Haartman Institute, University of Helsinki, Helsinki, Finland,2 Department of Medical Microbiology, University of Oulu, Oulu, Finland,3 National Public Health Institute, Oulu, Finland,4 Division of Infectious Diseases, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland5

Received 30 March 2007/ Returned for modification 16 July 2007/ Accepted 24 October 2007

The immune system may interplay between Chlamydia pneumoniae infection and coronary artery disease (CAD). Major histocompatibility complex genes regulate innate and adaptive immunity. Patients with CAD (n = 100) and controls (n = 74) were enrolled. Human leukocyte antigens (HLA-A, HLA-B, and HLA-DRB1), four lymphotoxin alpha single-nucleotide polymorphisms, and complement C4A and C4B allotypes were typed, and their haplotypes were inferred. The presence of serum C. pneumoniae immunoglobulin A (IgA) (titer, ≥40) or IgG (titer, ≥128) antibodies or immune complex (IC)-bound IgG antibodies (titer, ≥2) was considered to be a serological marker suggesting chronic C. pneumoniae infection. C. pneumoniae IgA antibodies were found more frequently in patients than in controls (P = 0.04). Among the patients, multiple logistic regression analysis showed the HLA-B*35 allele to be the strongest-risk gene for C. pneumoniae infection (odds ratio, 7.88; 95% confidence interval, 2.44 to 25.43; P = 0.0006). Markers of C. pneumoniae infection were found more frequently in patients with the HLA-A*03-B*35 haplotype than in those without the haplotype (P = 0.007 for IgA; P = 0.008 for IgG; P = 0.002 for IC). Smokers with HLA-B*35 or HLA-A*03-B*35 had markers of C. pneumoniae infection that appeared more often than in smokers without these genes (P = 0.003 and P = 0.001, respectively). No associations were found in controls. In conclusion, HLA-B*35 may be the link between chronic C. pneumoniae infection and CAD.

* Corresponding author. Mailing address: Division of Cardiology, Department of Medicine, Helsinki University Central Hospital, P.O. Box 340, FI-00029 Helsinki, Finland. Phone: 358-9-471 72442. Fax: 358-9-471 74574. E-mail: juha.sinisalo{at}hus.fi

{triangledown} Published ahead of print on 7 November 2007.

Clinical and Vaccine Immunology, January 2008, p. 55-59, Vol. 15, No. 1
1071-412X/08/$08.00+0     doi:10.1128/CVI.00163-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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