Lymphocyte responses to Chlamydia antigens in

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infection and coronary atherosclerosis we studied cell- mediated and humoral immune responses to Chlamydia in. 93 patients with angiographically confirmed ...
European Heart Journal (1997) 18, 1095-1101

Lymphocyte responses to Chlamydia antigens in patients with coronary heart disease S. Halme*§, H. Syrjalaf, A. Bloigu*, P. Saikku*§, M. Leinonen*, J. Airaksinent and H-M. Surcel* * National Public Health Institute, Oulu, and ^Departments of Infection Control and \Internal Medicine, Division of Cardiology, Oulu University Central Hospital, and ^Department of Medical Microbiology, University of Oulu, Oulu, Finland

Aims To clarify the relationship of Chlamydia pneumoniae infection and coronary atherosclerosis we studied cellmediated and humoral immune responses to Chlamydia in 93 patients with angiographically confirmed coronary heart disease and in 115 controls without angiographically demonstrable lesions.

Conclusion Marked cell-mediated and humoral immunity to C. pneumoniae in males with coronary heart disease suggest that the immune mechanisms triggered by Chlamydia are a possible contributing factor in the disease pathogenesis of coronary atherosclerosis in males. The Chlamydia-specific cell-mediated responses seem to be predominantly induced by antigenic structures that are similar among different Chlamydia-species. (Eur Heart J 1997; 18: 1095-1101) Key Words: Chlamydia pneumoniae, cell-mediated immunity, coronary heart disease.

Introduction

specific IgG, and especially IgA, antibodies and immune-complexes in their sera'5"12', which are considChlamydia pneumoniae is a common human respiratory ered as markers of chronic infection'5'10'. The presence pathogen world-wide'1>2'. C. pneumoniae-specific anti- of C. pneumoniae organism or its DNA in diseased bodies that develop during the infection are usually coronary arteries'13"17' has strengthened the concept lost in 2-5 years'31. However, the prevalence of C. that a chronic C. pneumoniae infection is involved in pneumoniae-specific antibodies increases with age and atherosclerosis. Recently, Muhlestein et a/.'181 showed is about 50% in middle-aged adults, suggesting that that Chlamydia was present in 73% of the coronary most people are infected with C. pneumoniae during arteries in patients with symptomatic atherosclerosis their lifetime and reinfections and persistent infections but only in 4% of controls with normal coronary are common'2'4'. The link between C. pneumoniae infec- arteries or transplant-induced coronary disease. The tion and atherosclerosis was found by seroepidemio- absence of Chlamydia in non-atherosclerotic though logical studies showing that, in comparison to age- or diseased coronary tissue was considered a strong sex-matched controls, coronary heart disease patients indication that Chlamydia infection played an aetiohave persistently elevated levels of C. pneumoniae- logical role in the development of coronary atherosclerosis'18'. Further studies are needed to clarify the Revision submitted 27 January 1997, and accepted 29 January role of C. pneumoniae infection as an initiator of the 1997. atherosclerotic process. Host immune responses to Chlamydia are poorly Correspondence: Dr H-M. Surcel, National Public Health Institute, P.O. Box 310, 90101 Oulu, Finland. understood but there is increasing evidence to show that 0195-668X/97/071095+07 $18.00/0

1997 The European Society of Cardiology

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Methods and results Cell-mediated responses were analysed by measuring lymphocyte proliferative reactivity to whole elementary body antigens of C. pneumoniae. Control antigens included C. trachomatis and purified protein derivative of tuberculin. Chlamydia-specihc antibodies were measured using microimmunofluorescence assay. Marked C. pneumoniae-specific immune reactivity, demonstrated by the high incidence of elevated IgG and IgA antibodies and strong lymphocyte proliferative response, was associated with coronary heart disease in male but not in female patients or controls. In male patients, the cellmediated responses were strong to C. pneumoniae (median

stimulation index 9,6) and to C. trachomatis (stimulation index 6,9). The females with coronary heart disease showed significantly stronger cell-mediated responses to C. pneumoniae (stimulation index 6,5) than to C. trachomatis (3,8; /)