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The study by van der Ven et al¹ showed antibodies to Chlamydia pneumoniae to be significantly associated with atherosclerosis and renovascular disease in patients with hypertension and a strongly suspected renal artery stenosis. The specific IgG or IgA antibodies used in the study, however, do not necessarily distinguish between persistence of real infections and only a previous contact. Specific IgG-containing immune complexes for C pneumoniae have been demonstrated to be more sensitive markers of a real infection.²

Because of these limitations, the authors' data do not really indicate that the infectious agent plays a direct role in atherosclerosis. The high prevalence of a seropositivity to C pneumoniae in patients with atherosclerosis may rather suggest a "bystander activation" of the immune system.³ Autoreactive T cells may exist in these subjects, representing a potential reservoir of pathogenic effectors that, when stimulated by microbial adjuvants, could trigger an autoimmune phenomenon. The induction of . . . [Full Text of this Article]

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