Chlamydia pneumoniae and atherosclerotic plaque.

To the Editor-According to Campbell et al. [1] in their recent study of Chlamydia pneumoniae in coronary tissue, staining with a Chlamydia-specific monoclonal antibody detected chlamydiae in 45% of the atherectomy specimens from patients with atherosclerotic plaque. However, staining appeared only in macrophages; smooth muscle cells did not stain, a result that appears to contradict previous findings by some of the same researchers [2]. This apparent difference is not explained in the recent publication [1]. The discrepancy might be due to the different activities of the lesion types used in the two studies. Patients in the most recent study had angina or acute myocardial ischemia (or both). According to Saikku et al. [3], such patients show reactivation of chronic C. pneumoniae infection and an increase of inflammatory activity in atherosclerotic plaque. In the inflammatory processes, the production of interferon-y by T lymphocytes increases, thus inhibiting the proliferation of the smooth muscle cells and activating apoptosis in these cells [4]. The speed of the apoptosis causes considerable cell loss, yet few cells are visualized in the destruction process [5]. The intense loss of smooth muscle cells in the active atherosclerotic plaque may also cause destruction of C. pneumoniaeinfected smooth muscle cells. Perhaps, by eliminating infected cells, accelerated apoptosis acts as a defense mechanism in chronic C. pneumoniae infection. The discrepancy between the two atherosclerosis studies [1, 2] might also be explained by other studies that more solidly associate