Atherogenetically relevant cells support continuous growth of Chlamydia pneumoniae

The obligate intracellular bacterium Chlamydia pneumoniae has been implicat ed in the pathogenesis of atherosclerosis since viable pathogen has been re covered from plaques. Chlamydiae are epithelial pathogens notorious for cau sing persistent infection. Atherosclerosis, however, is a chronic inflammat ory disease involving mesenchymal cells of the vascular wall. A bacterial c ontribution to atherosclerosis appears more relevant if the resident mesenc hymal cells of the vascular wall that constitute the prague can support chl amydial infection continuously. Therefore we inoculated immortalized and primary mesenchymal cells with a v ascular and a respiratory Chlamydia pneumoniae isolate. Primary human coron ary artery endothelial and smooth muscle cells, primary human embryonic fib roblasts as well as the immortalized cell lines were permissive for continu ous growth of both strains. Thus, the resident vascular cells that produce the atheromatous plaque can acquire permanent productive Chlamydia pneumoni ae infection. Immortalized monocytic cells and peripheral blood monocytes a lso supported chlamydial growth, though productive infection ceased after 5 passages. Monocytes/macrophages are not resident cells of the vascular wall but have an active role in plaque formation. Systemic circulation and transendotheli al migration makes them a potential vector system for chlamydial distributi on. These findings add further plausibility to the hypothesis of a chronic infectious component in the multifactorial condition of atherosclerosis. Fu rther studies must precisely define chlamydial target cells in vivo and dif ferentiate infection in resident cells of the vascular wall from a presence limited to migrating macrophages. Endovascular infection might provide an explanation for unclear phenomena of atherogenesis like mesenchymal cell pr oliferation and its distinct inflammatory component.