Lps-induced Inflammation
Lps-induced Inflammation - Related Videos
08:43
Investigating Intestinal Inflammation in DSS-induced Model of IBD
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Cited by 607 •
2012
Experimental models of inflammatory bowel disease have allowed us to examine the complex innate and adaptive immune responses associated with pathogenesis. Using histological scoring, quantification of pro-inflammatory cytokines and myeloperoxidase activity, one can begin to assess these responses seen in inflammatory bowel disease.
03:06
A Method to Induce Ocular Surface Inflammation in a Murine Model
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2025
This video demonstrates a method to induce ocular surface inflammation and meibomian gland dysfunction in a murine model. Stimulation of the mouse's immune system using an immunogen and later restimulation with the same immunogen promotes ocular surface inflammation, which causes plugging of meibomian gland secretion through neutrophil-produced aggNETs and leads to dry eye disease.
02:49
A Technique to Assess the Immune Response against an Antigen by Inducing Skin Inflammation
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2025
This video demonstrates an in vivo technique to assess a test antigen by inducing skin inflammation in a murine model. The test antigen—a hapten in an oil/acetone solution—is topically applied to the skin of the mouse ear, and inflammation of the skin is assessed after an adequate period.
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.
09:52
A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
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Cited by 15 •
2014
Animal models have proven to be invaluable tools in defining host and pathogen specific mechanisms that contribute to the development of chronic inflammation. Here we describe a mouse model of oral infection with the human pathogen Porphyromonas gingivalis and detail methodologies to assess the progression of inflammation at local and systemic sites.
FAQs
CD14 and the TLR4-MD-2 receptor complex act as recognition components for LPS on immune cells. Their engagement initiates intracellular signaling rather than producing inflammation directly at the cell surface. This receptor-level step is important because it connects detection of a Gram-negative bacterial component with downstream activation of transcription factors and inflammatory mediator production.
The MyD88- and TRIF-dependent pathways provide distinct signaling routes after receptor engagement. Together, they stimulate NF-κB and other transcription factors, which regulate expression of inflammatory genes. Considering both pathways helps researchers analyze how LPS detection is converted into cytokine production and how innate immune signaling coordinates an early response to infection-related stimuli.
The response is beneficial when inflammatory signaling helps initiate antimicrobial defense against Gram-negative bacteria. However, excessive activation can extend beyond local protection and produce systemic inflammation, which may injure tissues. This dual effect makes the process valuable for studying both effective innate immunity and the harmful consequences of uncontrolled inflammatory signaling.
Cytokines such as tumor necrosis factor and interleukins are key outputs of the signaling response. Their production indicates that receptor-triggered transcriptional programs have been activated in immune cells. Examining these mediators helps connect molecular events involving NF-κB and related transcription factors with the broader inflammatory state generated during host responses to LPS.
Researchers use LPS-induced inflammation to model inflammatory signaling in a controlled research context. The model links a defined bacterial component with receptor activation, intracellular pathways, and cytokine production. It therefore supports investigations of how host cells respond to microbial signals and provides a framework for examining mechanisms that may be difficult to isolate during complex infections.
In immunology and infection research, the model helps investigate host-pathogen interactions by examining how immune cells recognize and respond to a Gram-negative bacterial component. It is also used to evaluate potential treatments for sepsis and related disorders. These applications focus on reducing harmful systemic inflammation while preserving the protective functions of innate immune activation.