Abstract
Chlamydia pneumoniae is recognised as a common cause of respiratory tract infections and has recently been implicated in several extrapulmonary chronic diseases, with great impact on public health, such as atherosclerosis, multiple sclerosis and Alzheimer's disease. The involvement of C. pneumoniae in such diseases may be correlated to characteristic features of this pathogen, including intracellular growth and ability to induce persistent forms. C. pneumoniae persistent forms are inherently more suited to evade the host immune response and are more difficult to eradicate by antibiotics. Our preliminary experimental findings show that interaction of C. pneumoniae with macrophages and/or T cells characterized by interference with TNF-α production, and redox state, culminates in the induction of T cell apoptosis and survival of infected macrophages. Based on our evidence, the poor cooperation between T cells and macrophages could lead to an inappropriate immune response against C. pneumoniae that may therefore promote the development of extrapulmonary chronic diseases.