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Related Concept Videos

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...
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...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Regulation of Bacterial Virulence01:28

Regulation of Bacterial Virulence

Pathogenic bacteria employ a range of regulatory mechanisms to modulate the expression of virulence genes in response to environmental and host-derived signals. These mechanisms ensure that virulence factors are expressed only under favorable conditions, thereby optimizing infection and survival strategies.Mechanisms of Virulence RegulationKey regulatory strategies include:Two-Component Systems: These consist of a membrane-bound sensor kinase and a cytoplasmic response regulator. Environmental...
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...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.

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Updated: May 27, 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

AIP56: a novel bacterial apoptogenic toxin.

Manuel T Silva1, Nuno M S Dos Santos, Ana do Vale

  • 1IBMC-Instituto de Biologia Molecular e Celular, Rua do Campo Alegre, 823. 4150-180 Porto, Portugal. mtsilva@ibmc.up.pt

Toxins
|November 10, 2011
PubMed
Summary

Photobacterium damselae subsp. piscicida (Phdp) exotoxin AIP56 triggers fish immune cell apoptosis, leading to septicemia. This virulence factor causes disease pathology similar to natural infections in fish.

Keywords:
AB toxinAIP56Photobacterium damselae subsp. piscicidaapoptosissecondary necrosis

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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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Last Updated: May 27, 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

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 and Immunology
  • * Fish Pathology
  • * Bacterial Pathogenesis

Background:

  • * Photobacterium damselae subsp. piscicida (Phdp) is a Gram-negative bacterium causing significant fish septicemia.
  • * The plasmid-encoded exotoxin AIP56 is a primary virulence factor of Phdp, secreted during active bacterial growth.

Purpose of the Study:

  • * To investigate the role and mechanism of the exotoxin AIP56 in fish septicemia.
  • * To elucidate the effects of AIP56 on fish immune cells and its contribution to disease pathogenesis.

Main Methods:

  • * Analysis of AIP56 protein structure, including signal peptide and zinc-binding region.
  • * In vitro and in vivo studies assessing AIP56's impact on fish macrophages and neutrophils.
  • * Examination of apoptosis pathways (caspase-3, -8, -9) and secondary necrosis markers.

Main Results:

  • * AIP56 selectively induces apoptosis in fish macrophages and neutrophils via a caspase-dependent pathway.
  • * In vivo, AIP56-induced apoptosis leads to secondary necrosis and release of cytotoxic molecules like neutrophil elastase.
  • * Experimental infection with recombinant AIP56 mimics the pathology of natural Phdp septicemia.

Conclusions:

  • * AIP56 is a critical virulence factor responsible for the immunopathology of Phdp infections in fish.
  • * Targeting AIP56 or its downstream effects could offer strategies for controlling fish septicemia.