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Long-term memory is a relatively permanent type of memory, capable of storing vast amounts of information over extended periods. Its storage capacity is generally considered unlimited.
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Methods for Detecting Cytotoxic Amyloids Following Infection of Pulmonary Endothelial Cells by Pseudomonas aeruginosa
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Methods for Detecting Cytotoxic Amyloids Following Infection of Pulmonary Endothelial Cells by Pseudomonas aeruginosa

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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.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|June 19, 2019
PubMed
Summary
This summary is machine-generated.

Nosocomial pneumonia can lead to brain dysfunction. Bacterial infection of the endothelium releases amyloid and tau proteins, impairing memory and synaptic plasticity in mice.

Keywords:
cerebrospinal fluiddementiadepressionlearningnosocomial pneumonia

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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.