Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Pneumonia I: Introduction01:29

Pneumonia I: Introduction

Pneumonia is an infection of the lower respiratory tract that leads to inflammation of the lung parenchyma, often resulting in the accumulation of inflammatory exudate in the alveoli and airways. Unlike the watery, low-protein fluid exudate in pulmonary edema, the exudate in this case is a thick fluid rich in immune cells, proteins, and debris produced during infection and inflammation.This impairs gas exchange and can lead to consolidation of lung tissue. The infection may be caused by a...
Pneumonia I: Introduction01:30

Pneumonia I: Introduction

Pneumonia is an acute respiratory infection that targets the lungs, specifically the alveoli. These tiny air sacs, essential for oxygen exchange, become engorged with pus and fluid, severely hindering breathing, decreasing oxygen absorption, and causing significant pain and discomfort during respiration.
Risk Factors
Various factors influence the likelihood of developing pneumonia. Age plays a crucial role, with infants, children under two, and individuals over 65 at increased risk due to their...
Botulism01:22

Botulism

Botulism is a life-threatening neuroparalytic condition caused by botulinum neurotoxin, which is produced by the bacterium Clostridium botulinum, a Gram-positive, spore-forming, obligate anaerobe.In adults, the toxin enters the body in different ways: in foodborne botulism, the preformed toxin is absorbed in the intestine. In wound botulism, spores grow in injured tissue and release the toxin into the blood. Infant botulism differs mechanistically from adult forms. In infants, botulism commonly...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
Pneumonia II: Pathophysiology01:29

Pneumonia II: Pathophysiology

The pathophysiology of pneumonia involves the following steps:

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Expression of GPR34 in microglia remains stable in human Alzheimer's disease.

Acta neuropathologica·2026
Same author

A deep-learning framework reveals whole-body perturbations at cell level.

Nature·2026
Same author

Diet-Driven Microglial Activation: Region-Specific Neuroinflammation in the Mouse Brain.

Brain sciences·2026
Same author

Non-hematopoietic erythropoietin splice variant is produced in the diseased human brain and confers neuroprotection.

Frontiers in cellular neuroscience·2026
Same author

Modulating food intake by nasal application of peptides targeting melanocortin 4 receptor and ghrelin receptor systems.

Brain communications·2026
Same author

Proteomic comparison of human brain tissue preservation methods.

Journal of proteomics·2026

Related Experiment Video

Updated: Jul 14, 2026

Methods for Detecting Cytotoxic Amyloids Following Infection of Pulmonary Endothelial Cells by Pseudomonas aeruginosa
07:27

Methods for Detecting Cytotoxic Amyloids Following Infection of Pulmonary Endothelial Cells by Pseudomonas aeruginosa

Published on: July 12, 2018

Pneumolysin causes neuronal cell death through mitochondrial damage.

Johann S Braun1, Olaf Hoffmann, Miriam Schickhaus

  • 1Department of Neurology, Charité Universitaetsmedizin Berlin, Berlin, Germany. johannb@uaeu.ac.ae

Infection and Immunity
|June 15, 2007
PubMed
Summary

Pneumolysin, a toxin from Streptococcus pneumoniae, causes neuronal cell death by damaging mitochondria and inducing apoptosis independently of caspases. Blocking this toxin may protect against meningitis.

More Related Videos

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
10:36

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons

Published on: November 6, 2017

Related Experiment Videos

Last Updated: Jul 14, 2026

Methods for Detecting Cytotoxic Amyloids Following Infection of Pulmonary Endothelial Cells by Pseudomonas aeruginosa
07:27

Methods for Detecting Cytotoxic Amyloids Following Infection of Pulmonary Endothelial Cells by Pseudomonas aeruginosa

Published on: July 12, 2018

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
10:36

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons

Published on: November 6, 2017

Area of Science:

  • Microbiology
  • Neuroscience
  • Cell Biology

Background:

  • Pneumolysin is a key cytotoxic factor released by Streptococcus pneumoniae, a primary cause of bacterial meningitis.
  • Bacterial toxins mediate cytotoxicity in infections, but their precise mechanisms in neuronal cell death are not fully elucidated.

Purpose of the Study:

  • To investigate the role of pneumolysin in Streptococcus pneumoniae-induced neuronal cell death pathways.
  • To determine the mechanism by which pneumolysin induces apoptosis in primary neurons.

Main Methods:

  • Primary neuron cultures were treated with live bacteria, purified pneumolysin, or pneumolysin-negative bacteria.
  • Mitochondrial membrane potential, apoptosis-inducing factor release, and caspase activation were assessed.
  • Expression of X-chromosome-linked inhibitor of apoptosis protein was analyzed.

Main Results:

  • Pneumolysin is the primary pneumococcal factor responsible for inducing apoptosis in primary neurons.
  • Pneumolysin's pore-forming activity is essential for mitochondrial damage and subsequent apoptosis, independent of caspase activation.
  • Pneumolysin directly targets mitochondria, altering membrane potential and releasing apoptosis-inducing factors, while also upregulating X-chromosome-linked inhibitor of apoptosis protein.

Conclusions:

  • Pneumolysin functions as a mitochondrial toxin and drives caspase-independent apoptosis in neurons.
  • Blocking pneumolysin presents a potential cytoprotective strategy for pneumococcal meningitis and other related infections.