Chlamydia Pneumoniae (C. Pn) is an obligatory intracellular bacterium that is associated with
respiratory tract infections like
pneumonia,
pharyngitis and
bronchitis. It has also been implicated in
cerebrovascular (stroke) as well as
cardiovascular diseases. The most possible pathway via which C. Pn elicits its pathogenesis could be via activation of Human Vascular Smooth Muscle Cells (VSMCs) proliferation resulting in the stimulation of Toll-Like Receptor-4 (TLR-4) and/or phospho-44/42(p44/p42)
Mitogen-Activated Protein Kinases (MAPK). It is also established that
tyrosine phosphorylation of IQ domain
GTPase-activating protein 1 (IQGAP1) also contributed to C. Pn
infection-triggered Vascular Endothelial Cell (VEC) movements via the
SRC tyrosine kinase inhibitor PP2 (4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]
pyrimidine) resulting in angiogenesis. It is also proven that restricted inflammatory cell infiltrates as well as apoptosis have been linked to C. Pn or C. Pn-specific
proteins in
atherosclerotic plaques of patients with
stroke. It is further an evidence that C. Pn enters the cerebral vasculature during the initial
infection and worsen
atherosclerosis either directly or indirectly. Chronic, persistent C. Pn
infection is also capable of triggering the secretion of Chlamydial
Heat Shock Protein 60 (cHSP60) in the vessel wall resulting in augmentation of
inflammation. C. Pn also
aids in the activation of explicit cell-intermediated immunity within plaques. Macrophages in the carotid plaques co-exist with CD4+ lymphocytes which are capable of triggering the release of pro-inflammatory
cytokines resulting in the augmentation of atherogenic development during C. Pn
infection. C. Pn actively participated in the modification of both
histones H3 and H4 during
chromatin analysis via the
interleukin 8(IL-8) gene facilitator as well as conscription of
nuclear factor kappa-B(NF-κB) or NF- κB/p65 complex and polymerase II (Pol II). This review, therefore, focuses on the crucial involvement of C. Pn in the pathogenesis of cerebrovascular events.