Title:Pivotal Pathogenic and Biomarker Role of Chlamydia Pneumoniae in Neurovascular Diseases
Volume: 15
Issue: 3
Author(s): Seidu A. Richard *
Affiliation:
- Department of Surgery, Volta Regional Hospital, P.O. Box MA-374, Ho,Ghana
Keywords:
Chlamydia Pneumoniae (C. Pn), pneumonia, stroke, angiogenesis, atherosclerosis, neurovascular diseases.
Abstract: 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.
