Huvec Infection
Huvec Infection - Related Videos
09:19
Isolation of Human Umbilical Vein Endothelial Cells (HUVEC)
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Cited by 131 •
2007
This video protocol illustrates the isolation and culture of human umbilical vein endothelial cells (HUVEC) from human umbilical cord. Once isolated these cells can be used for in vitro angiogenesis assays like the Optimized Fibrin Gel Bead Assay also demonstrated by the Hughes lab.
05:28
A Bacterial Infection Assay for Studying Anaerobic Bacteria-Host Cell Interactions
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2025
This video demonstrates a technique for assessing the ability of Porphyromonas gingivalis, an anaerobic pathogenic bacterium, to adhere to and invade human umbilical vein endothelial cells (HUVECs). After infecting the host cells with the bacteria, the host cells are lysed to release both adhered and internalized bacteria. When the lysate is plated in an appropriate medium, the presence of colonies indicates successful bacteria-host cell interactions.
06:12
HUVEC Tube-formation Assay to Evaluate the Impact of Natural Products on Angiogenesis
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Cited by 37 •
2019
Here, we evaluate the effects of the water extract of Ruta graveolens on vessel network formation by using a tube formation assay on a gelled basement matrix.
12:30
Use of Galleria mellonella as a Model Organism to Study Legionella pneumophila Infection
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Cited by 108 •
2013
The larva of the wax moth Galleria mellonella was recently established as an in vivo model to study Legionella pneumophila infection. Here, we demonstrate fundamental techniques to characterize the pathogenesis of Legionella in the larvae, including inoculation, measurement of bacterial virulence and replication as well as extraction and analysis of infected hemocytes.
07:59
Bioluminescence Imaging to Detect Late Stage Infection of African Trypanosomiasis
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Cited by 3 •
2016
This manuscript describes the use of a bioluminescent strain of African trypanosomes to enable the tracking of late stage infection and demonstrates how in vivo live imaging can be used to visualize infections within the central nervous system in real-time.
FAQs
The infection sequence can be examined as a progression from pathogen attachment to cellular entry and, when supported by the system, replication. Each stage can alter endothelial behavior, allowing investigators to relate pathogen-cell interactions to downstream cytokine release, adhesion-molecule changes, or impaired barrier integrity. This links early cellular events with vascular inflammation rather than treating infection as a single endpoint.
Changes in cytokine release and adhesion molecules can make the endothelial surface more supportive of leukocyte recruitment. If barrier integrity is also lost, vascular inflammation and injury become important outcomes to examine. Together, these readouts connect local pathogen interaction with broader inflammatory effects in the vessel wall, which is especially relevant to immunology and infection studies.
The infectious agent and the experimental conditions shape how endothelial cells respond. One setup may emphasize pathogen attachment or entry, whereas another may reveal stronger cytokine release, adhesion-molecule changes, or barrier disruption. Interpreting results therefore requires relating each observed response to the defined pathogen and conditions used, rather than assuming that every infection produces the same vascular effect.
These stages represent different points in the host-pathogen interaction and can have different consequences for endothelial cells. Separating them helps investigators determine whether a response is associated mainly with initial contact, cellular entry, or continued pathogen activity. That distinction improves analysis of how infection progresses toward inflammatory signaling, altered adhesion properties, or loss of barrier integrity.
A typical workflow begins with cultured HUVECs and exposure to a defined pathogen. Researchers then examine the resulting interaction and endothelial responses, including attachment, cellular entry or replication, cytokine release, adhesion-molecule changes, and barrier integrity. Organizing the experiment around these linked stages allows the model to connect pathogen behavior with measurable effects on vascular endothelial function.
The model can provide information about both pathogen activity and host-cell responses. Relevant outcomes include whether attachment, cellular entry, or replication occurs; whether cytokine release changes; whether adhesion molecules are altered; and whether barrier integrity is lost. Taken together, these measurements describe how infection may influence leukocyte recruitment and vascular inflammation.
This model is useful when investigators need to study host-pathogen interactions at the vascular endothelium or examine mechanisms of vascular injury. It can also support evaluation of antimicrobial and anti-inflammatory treatments. By linking infection-related cellular events to cytokine, adhesion, and barrier responses, the system helps assess both disease mechanisms and treatment-associated changes.