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

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
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...
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...

You might also read

Related Articles

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

Sort by
Same author

Protein tyrosine kinases in dendritic cell-mediated anti-cancer immunity.

Seminars in immunology·2026
Same author

Trial watch: antibody-drug conjugates in cancer therapy.

Oncoimmunology·2026
Same author

The autophagy-inhibitory tissue hormone DBI/ACBP is essential for glucocorticoid-induced immunosuppression.

Autophagy·2026
Same author

Restoring dendritic cell migration: a gut reaction to boost vaccine efficacy in aging.

Oncoimmunology·2026
Same author

Pharmacological inhibition of MAPK P38α rescues the immune defect of dendritic cells affected by the FPR1 loss-of-function polymorphism rs867228.

Oncoimmunology·2026
Same author

High-throughput cell viability assessment using a luminescent ATP detection assay.

Methods in cell biology·2026
Same journal

Waterborne diseases and climate change.

Nature reviews. Microbiology·2026
Same journal

Climate adaptation and biodiversity shape West Nile virus risk in cities.

Nature reviews. Microbiology·2026
Same journal

Climate factors and evolution drive cholera surges in Dhaka.

Nature reviews. Microbiology·2026
Same journal

Climate change boosts Salmonella antimicrobial resistance.

Nature reviews. Microbiology·2026
Same journal

Reframing risk assessment for malaria elimination in a changing climate.

Nature reviews. Microbiology·2026
Same journal

Bacterial vesicles protect the membrane during polymyxin stress.

Nature reviews. Microbiology·2026
See all related articles

Related Experiment Video

Updated: Jun 9, 2026

Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling
08:51

Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling

Published on: June 25, 2015

Interactions between bacterial pathogens and mitochondrial cell death pathways.

Thomas Rudel1, Oliver Kepp, Vera Kozjak-Pavlovic

  • 1Lehrstuhl für Mikrobiologie, Biozentrum der Universität Würzburg, Germany. thomas.rudel@biozentrum.uni-wuerzburg.de

Nature Reviews. Microbiology
|September 7, 2010
PubMed
Summary
This summary is machine-generated.

Bacteria manipulate host cell death by targeting mitochondria. This review details how bacterial proteins interact with mitochondria to control cell fate, impacting disease.

More Related Videos

Real-Time Measurement of the Mitochondrial Bioenergetic Profile of Neutrophils
09:39

Real-Time Measurement of the Mitochondrial Bioenergetic Profile of Neutrophils

Published on: June 2, 2023

Related Experiment Videos

Last Updated: Jun 9, 2026

Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling
08:51

Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling

Published on: June 25, 2015

Real-Time Measurement of the Mitochondrial Bioenergetic Profile of Neutrophils
09:39

Real-Time Measurement of the Mitochondrial Bioenergetic Profile of Neutrophils

Published on: June 2, 2023

Area of Science:

  • Microbiology and Cell Biology
  • Pathogenesis and Host-Pathogen Interactions

Background:

  • Bacterial pathogenicity often involves manipulating host cell death pathways.
  • Mitochondria are key organelles in regulating cell life and death decisions.
  • Bacterial pathogens have evolved mechanisms to interfere with host mitochondrial functions.

Purpose of the Study:

  • To review the intricate interactions between bacterial pathogens and host mitochondrial cell death pathways.
  • To highlight how bacteria hijack mitochondrial signaling to promote survival or virulence.

Main Methods:

  • Literature review of studies on bacterial-host interactions.
  • Analysis of known bacterial proteins that target mitochondria.
  • Examination of signaling pathways converging on mitochondria.

Main Results:

  • Bacterial proteins specifically interact with host mitochondria.
  • These interactions modulate mitochondrial function and cell death.
  • Pathogens exploit these interactions for their own benefit.

Conclusions:

  • Targeting mitochondrial cell death is a critical bacterial pathogenicity mechanism.
  • Understanding these interactions offers insights into novel therapeutic strategies.