Related Experiment Video

Updated: May 28, 2026

Legionella pneumophila Outer Membrane Vesicles: Isolation and Analysis of Their Pro-inflammatory Potential on Macrophages
08:34

Legionella pneumophila Outer Membrane Vesicles: Isolation and Analysis of Their Pro-inflammatory Potential on Macrophages

Published on: February 22, 2017

Vibrio vulnificus outer membrane vesicles induce mitochondrial dysfunction in macrophages via the TNF signaling

Jun Li1, Luying Wang1, Yafang Zhou1

  • 1Key Laboratory of Laboratory Medicine, Ministry of Education, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, China.

Frontiers in Veterinary Science
|May 27, 2026
PubMed

Insights

Vibrio vulnificus outer membrane vesicles (OMVs) trigger inflammation and mitochondrial damage in macrophages by activating TNF signaling. Blocking TNF receptors reduces this injury, revealing a new mechanism of V. vulnificus pathogenesis.

Area of Science:

  • Microbiology
  • Immunology
  • Pathogenesis

Background:

  • Vibrio vulnificus causes severe human infections with a cytokine storm.
  • Bacterial outer membrane vesicles (OMVs) mediate host-pathogen interactions.
  • The role of V. vulnificus OMVs in immunopathology is unclear.

Purpose of the Study:

  • Isolate and characterize V. vulnificus OMVs.
  • Investigate their impact on murine macrophages.
  • Elucidate the underlying pathogenic mechanisms.

Main Methods:

  • OMV isolation and characterization.
  • Macrophage internalization assays.
  • Transcriptomic analysis (TNF signaling, NF-κB, MAPK).
  • Mitochondrial function assessment (membrane potential, ultrastructure).
  • Pharmacological inhibition of TNF receptor.

Main Results:

  • V. vulnificus OMVs are internalized by macrophages, inducing pro-inflammatory responses.
  • OMVs activate the TNF signaling pathway, phosphorylating NF-κB and MAPK.
  • OMV exposure causes significant mitochondrial dysfunction.
  • TNF receptor blockade attenuates OMV-induced mitochondrial damage.

Conclusions:

  • V. vulnificus OMVs utilize the TNF signaling axis to induce mitochondrial injury.
  • This represents a novel pathogenic mechanism contributing to V. vulnificus lethality.
  • The TNF-mitochondria axis is a potential therapeutic target against V. vulnificus infections.
Keywords:
TNF-αVibrio vulnificusmacrophagesmitochondrial dysfunctionouter membrane vesicles (OMVs)

More Related Videos

Visualization of Vascular Ca2+ Signaling Triggered by Paracrine Derived ROS07:33

Visualization of Vascular Ca2+ Signaling Triggered by Paracrine Derived ROS

Published on: December 21, 2011

Determination of Tolerable Fatty Acids and Cholera Toxin Concentrations Using Human Intestinal Epithelial Cells and BALB/c Mouse Macrophages09:39

Determination of Tolerable Fatty Acids and Cholera Toxin Concentrations Using Human Intestinal Epithelial Cells and BALB/c Mouse Macrophages

Published on: May 30, 2013

Related Concept Videos

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...
Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
Porin Insertion in the Outer Mitochondrial Membrane01:12

Porin Insertion in the Outer Mitochondrial Membrane

Porins are beta-barrel proteins translocated to the mitochondrial outer membrane through the TOM complex into the intermembrane space. Porin precursors bind TIM chaperones within the intermembrane space and are guided to the Sorting and Assembly Machinery complex or SAM complex on the outer mitochondrial membrane.
Three models describe the assembly of porins by the SAM complex and their insertion into the outer membrane. Model 1 suggests that porins are assembled outside the SAM channel as the...
Mitochondrial Membranes01:45

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
Mitochondrial Membranes01:45

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...