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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...
Bacterial Toxins01:12

Bacterial Toxins

Bacterial toxins are sophisticated virulence factors that enable pathogenic bacteria to interact with, invade, and damage host tissues. These toxins fall broadly into two types: protein exotoxins, which are secreted into the environment and target specific host receptors, and lipopolysaccharide endotoxins, which are structural components of the bacterial outer membrane released primarily during bacterial lysis or membrane shedding. Exotoxins generally act more selectively, binding to cell...
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,...
Receptor-mediated Endocytosis01:20

Receptor-mediated Endocytosis

Receptor-mediated endocytosis is when bulk amounts of specific molecules are imported into a cell after binding to cell surface receptors. The molecules bound to these receptors are taken into the cell through inward folding of the cell surface membrane, which is eventually pinched off into a vesicle within the cell. Structural proteins, such as clathrin, coat the budding vesicle.
Clathrin-Mediated Endocytosis of LDL
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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
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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.
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Related Experiment Video

Updated: May 16, 2026

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
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LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

Published on: May 3, 2024

A bacterial RTX toxin causes programmed necrotic cell death through calcium-mediated mitochondrial dysfunction.

Young Ran Kim1, Shee Eun Lee, In-Chol Kang

  • 1Clinical Vaccine R&D Center, Department of Microbiology, Chonnam National University Medical School, 5 Hak-Dong, Dong-Gu, Gwangju 501–746, Korea.

The Journal of Infectious Diseases
|December 11, 2012
PubMed
Summary

Vibrio vulnificus RtxA1 toxin causes cell death by forming pores and disrupting calcium homeostasis. This leads to mitochondrial dysfunction and cell lysis, crucial for V. vulnificus pathogenesis.

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Visualization of Bacterial Toxin Induced Responses Using Live Cell Fluorescence Microscopy
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Visualization of Bacterial Toxin Induced Responses Using Live Cell Fluorescence Microscopy

Published on: October 1, 2012

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LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
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Visualization of Bacterial Toxin Induced Responses Using Live Cell Fluorescence Microscopy
14:29

Visualization of Bacterial Toxin Induced Responses Using Live Cell Fluorescence Microscopy

Published on: October 1, 2012

Area of Science:

  • Microbiology
  • Cell Biology
  • Toxicology

Background:

  • Vibrio vulnificus is a bacterium causing severe infections.
  • The RtxA1 toxin is essential for V. vulnificus pathogenesis.
  • RtxA1 toxin mediates host cell death upon bacterial contact.

Purpose of the Study:

  • Elucidate the mechanism of RtxA1 toxin-mediated HeLa cell death.
  • Investigate RtxA1 toxin processing and localization within host cells.
  • Determine the role of calcium and mitochondrial pathways in RtxA1-induced cytotoxicity.

Main Methods:

  • Confocal microscopy to visualize toxin fragments.
  • Immunoblot analysis to detect toxin processing.
  • Measurement of intracellular calcium concentrations.
  • Assessment of mitochondrial membrane potential and ATP levels.

Main Results:

  • RtxA1 toxin is cleaved into RtxA1-N (membrane-bound) and RtxA1-C (cytoplasmic) fragments.
  • RtxA1-N likely forms pores, increasing intracellular calcium.
  • Increased Ca(2+) activates JNK and triggers calcium-dependent mitochondrial death pathways.
  • Mitochondrial dysfunction, ATP depletion, and plasma membrane damage occur.

Conclusions:

  • RtxA1 toxin induces cell death through a calcium-dependent mitochondrial pathway.
  • Toxin-mediated pore formation and subsequent calcium influx are critical.
  • This mechanism contributes significantly to V. vulnificus-induced cytotoxicity and pathogenesis.