Related Experiment Video

Updated: Sep 6, 2026

A Choroid Plexus Epithelial Cell-based Model of the Human Blood-Cerebrospinal Fluid Barrier to Study Bacterial Infection from the Basolateral Side
09:58

A Choroid Plexus Epithelial Cell-based Model of the Human Blood-Cerebrospinal Fluid Barrier to Study Bacterial Infection from the Basolateral Side

Published on: May 6, 2016

Chlamydia pneumoniae infection alters the junctional complex proteins of human brain microvascular endothelial cells

Angela MacIntyre1, Christine J Hammond, C Scott Little

  • 1Department of Biomedical Sciences, Philadelphia College of Osteopathic Medicine, 4170 City Ave, Philadelphia, PA 19131, USA.

FEMS Microbiology Letters
|December 14, 2002
PubMed

Insights

Chlamydia pneumoniae infection impacts blood-brain barrier integrity by altering key junctional proteins in brain endothelial cells. This finding offers insights into neuroinflammatory diseases like multiple sclerosis and Alzheimer's disease.

Area of Science:

  • Neuroscience
  • Infectious Diseases
  • Cell Biology

Background:

  • Chlamydia pneumoniae is linked to neurodegenerative diseases like multiple sclerosis (MS) and Alzheimer's disease (AD), but its role is debated.
  • Infection may compromise the blood-brain barrier (BBB), a critical protective layer for the brain.
  • The bacterium's potential to affect endothelial cells and BBB integrity is a key area of investigation.

Purpose of the Study:

  • To investigate the effect of Chlamydia pneumoniae infection on human brain microvascular endothelial cells (HBMECs).
  • To determine if C. pneumoniae alters the expression of proteins crucial for BBB integrity.
  • To explore a potential mechanism for C. pneumoniae's involvement in neuropathologies.

Main Methods:

  • Infection of HBMECs with C. pneumoniae.
  • Immunocytochemistry and Western blot analyses to assess protein expression.
  • Quantification of zonula adherens and tight junctional proteins.

Main Results:

  • C. pneumoniae infection increased the expression of beta-catenin, N-cadherin, and VE-cadherin (zonula adherens proteins).
  • Infection led to decreased expression of occludin, a tight junctional protein.
  • These changes suggest alterations in endothelial cell junctions and paracellular permeability.

Conclusions:

  • C. pneumoniae infection disrupts the expression of key proteins in brain endothelial cells.
  • These alterations may compromise BBB integrity and contribute to neuropathologies like MS and AD.
  • The study provides a potential mechanism for how C. pneumoniae influences neuroinflammation and disease progression.

More Related Videos

Neisseria meningitidis Infection of Induced Pluripotent Stem-Cell Derived Brain Endothelial Cells10:12

Neisseria meningitidis Infection of Induced Pluripotent Stem-Cell Derived Brain Endothelial Cells

Published on: July 14, 2020

Manual Segmentation of the Human Choroid Plexus Using Brain MRI04:25

Manual Segmentation of the Human Choroid Plexus Using Brain MRI

Published on: December 15, 2023

Related Concept Videos

Cryptococcal Meningitis01:27

Cryptococcal Meningitis

Cryptococcal meningitis is a life-threatening opportunistic infection predominantly associated with HIV/AIDS, accounting for over 100,000 deaths annually worldwide. However, it also affects individuals with other forms of immunosuppression, including those undergoing immunosuppressive therapy, organ transplant recipients, patients with innate immunodeficiencies, and individuals with hematological disorders. The infection is caused mainly by Cryptococcus neoformans and Cryptococcus gattii,...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
Encephalitis l: Introduction01:19

Encephalitis l: Introduction

Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...