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Updated: Jan 23, 2026
07:27
Methods for Detecting Cytotoxic Amyloids Following Infection of Pulmonary Endothelial Cells by Pseudomonas aeruginosa
Published on: July 12, 2018
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Infection-induced endothelial amyloids impair memory.
Ron Balczon1,2, Jean-Francois Pittet3, Brant M Wagener3
1Department of Biochemistry and Molecular Biology, University of South Alabama, Mobile, Alabama, USA.
Summary
Nosocomial pneumonia can lead to brain dysfunction. Bacterial infection of the endothelium releases amyloid and tau proteins, impairing memory and synaptic plasticity in mice.
Area of Science:
- Neuroscience
- Infectious Diseases
- Cell Biology
Background:
- Patients with nosocomial pneumonia show increased neurotoxic amyloid and tau proteins in cerebrospinal fluid (CSF).
- Pulmonary endothelium infected with bacteria like Pseudomonas aeruginosa, Klebsiella pneumoniae, or Staphylococcus aureus releases cytotoxic amyloid and tau proteins.
- The impact of these endothelium-derived proteins on brain function remains unclear.
Purpose of the Study:
- To investigate the effects of pulmonary endothelium-derived amyloid and tau proteins on brain function.
- To determine if Pseudomonas aeruginosa infection in mice leads to neurotoxicity and cognitive deficits.
- To elucidate the mechanism by which bacterial pneumonia may cause neurological complications.
Main Methods:
- Infection of mouse pulmonary endothelium with Pseudomonas aeruginosa (PA103 and ΔPcrV mutant).
- Intracerebroventricular injection of endothelium-derived proteins into mice.
- Behavioral testing (object recognition, fear conditioning, Morris water maze) and electrophysiological recordings (hippocampal slices).
- Immunodepletion of amyloid and tau proteins using specific antibodies (A11, T22).
Main Results:
- P. aeruginosa infection caused tau protein accumulation in the mouse brain and inhibited synaptic plasticity.
- Mice injected with endothelium-derived proteins showed learning and memory deficits.
- Supernatant from PA103 (intact type 3 secretion system) impaired working memory, while ΔPcrV supernatant (defective system) did not.
- Immunodepletion of amyloid or tau rescued working memory deficits.
- Endothelium-derived neurotoxins disrupted postsynaptic responses in hippocampal slices.
Conclusions:
- Bacterial infection of the pulmonary endothelium releases neurotoxic amyloid and tau proteins.
- These proteins can cross into the brain, causing synaptic dysfunction and cognitive deficits.
- A plausible mechanism for neurological complications following nosocomial pneumonia is established.
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