Lps Injection
Lps Injection - Related Videos
08:51
Intraductal Injection of LPS as a Mouse Model of Mastitis: Signaling Visualized via an NF-κB Reporter Transgenic
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Cited by 14 •
2012
Described here is a technique in which lipopolysaccharide is injected into the lactating mouse mammary gland via the nipple to simulate mastitis, a condition commonly caused by bacterial infection. Lipopolysaccharide injection results in increased nuclear factor kappa B (NF-κB) signaling, visualized through bioluminescent imaging of an NF-κB luciferase reporter mouse.
02:28
Inducing Neuroinflammation in Zebrafish Larvae with a Lipopolysaccharide Injection
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2025
The video demonstrates the microinjection of lipopolysaccharides (LPS) into the brains of zebrafish larvae to induce neuroinflammation. The larvae are positioned on an agarose-lined dish, the needle is inserted into the brain ventricles, and the LPS is injected. The injected LPS triggers an immune response that leads to neuroinflammation.
02:34
Intraperitoneal Injection of Bacterial Lipopolysaccharide in Mice to Study Systemic Immune Responses
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2026
Source: Radulovic, K., et al. Injections of Lipopolysaccharide into Mice to Mimic Entrance of Microbial-derived Products After Intestinal Barrier Breach. J. Vis. Exp. (2018)This video demonstrates a step-by-step procedure for injecting lipopolysaccharide (LPS) into mice intraperitoneally to induce systemic inflammation.
06:12
LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
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Cited by 1 •
2024
This protocol is based on LPS and ATP-induced death of PMA-differentiated THP-1 macrophages. We use flow cytometry to analyze Annexin V and 7-AAD double staining to detect cell death, using the whole cell and employing scanning electron microscopy to observe the cell membrane morphology.
08:28
Zebrafish Brain Ventricle Injection
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Cited by 72 •
2009
After neural tube formation, the neuroepithelium constricts and folds while the tube fills with embryonic cerebrospinal fluid (eCSF) to form the embryonic brain ventricles. We developed this ventricle injection technique to better visualize the fluid filled space in contrast to the neuroepithelial shape in a live embryo.
FAQs
LPS activates innate immune signaling through the coordinated action of the CD14, MD-2, and TLR4 receptor complex. This receptor interaction initiates cytokine production and other inflammatory pathways, creating a measurable immune challenge. In neuroscience experiments, the resulting signaling provides a basis for examining how peripheral inflammation may influence brain function and behavior.
The CD14–MD-2–TLR4 complex is important because it links recognition of LPS with downstream inflammatory signaling. Its activation helps explain why the same experimental challenge can produce both immune and neural consequences. Studying this receptor pathway allows researchers to connect cytokine responses with changes in brain function, cognition, mood, or behavior.
Dose, route, timing, and species can substantially change the magnitude and character of the response to LPS injection. These variables influence how strongly inflammation develops and how it relates to neural or behavioral outcomes. Consequently, researchers must interpret findings within the specific experimental conditions rather than assuming that results transfer unchanged across models.
Systemic inflammation can be associated with inflammatory changes affecting brain function, including alterations in cognition, mood, and sickness behavior. LPS studies are useful because they place immune activation and neural outcomes within the same experimental framework. This connection helps investigators examine how inflammatory signals relate to observable behavioral changes without treating those outcomes as independent processes.
A useful experimental description should identify the LPS dose, administration route, timing, and species, because each can shape the inflammatory response. Researchers should also distinguish the intended outcome, such as systemic inflammation, neuroinflammation, sickness behavior, cognition, or mood. Specifying these elements improves interpretation and makes comparisons between experiments more meaningful.
These models can provide information about immune activation alongside changes in brain function and behavior. Depending on the study design, investigators may examine neuroinflammation, sickness behavior, cognition, mood, or inflammation-associated neural effects. The approach also supports evaluation of potential therapeutic interventions by testing whether an intervention changes outcomes linked to the inflammatory challenge.