Lipopolysaccharide Induced Inflammation
Lipopolysaccharide Induced Inflammation - Related Videos
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.
03:41
An Air Pouch Mouse Model for Lipopolysaccharide-Induced Inflammatory Exudate Collection
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2025
This video describes the procedure for generating an air pouch in the subcutaneous tissue of mice and collecting inflammatory exudates in response to lipopolysaccharide administration in vivo. This video also covers the analysis of the neutrophil infiltration in the air pouch.
02:38
Lipopolysaccharide-Induced Acute Lung Injury in Mice for Exosome and Immune Analysis
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2026
Source: Yuan, Z., et al. Bronchoalveolar Lavage Exosomes in Lipopolysaccharide-induced Septic Lung Injury. J. Vis. Exp. (2018)This video demonstrates an in vivo mouse model for inducing and analyzing acute lung injury (ALI) using intraperitoneal administration of bacterial lipopolysaccharide. The inflammatory cascade triggered by alveolar macrophages and neutrophils leads to epithelial and endothelial barrier disruption, allowing fluid and immune cells to accumulate in the alveoli. Alveolar...
04:10
Non-Invasive Endotracheal Administration of Lipopolysaccharide to Induce Acute Lung Injury in Rodents
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2025
In this study, a non-invasive endotracheal instillation technique is demonstrated to develop ALI in rats using a basic laryngoscope to ensure precise LPS delivery to the lungs. The LPS is instilled via an endotracheal tube using a laryngoscope. The magnitude of lung injury is evaluated at multiple time points.
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.
FAQs
LPS recognition by CD14 and the MD-2-TLR4 receptor complex initiates intracellular signaling that activates NF-κB. This transcriptional pathway increases expression of inflammatory mediators, including tumor necrosis factor and interleukins. The receptor-to-transcription pathway explains how detection of a bacterial membrane component becomes a coordinated immune response capable of mobilizing host defenses.
The outcome depends on the intensity and extent of immune activation. A controlled response helps mobilize defenses against Gram-negative bacterial infection, whereas excessive signaling can produce widespread inflammation and tissue injury. When this response becomes systemic, it is associated with septic shock, illustrating how the same protective mechanism can become harmful.
Tumor necrosis factor and interleukins are among the cytokines produced after LPS activates immune-cell signaling. Their release helps communicate the presence of an inflammatory threat and coordinate host defenses. Measuring these cytokine responses can therefore indicate the strength of innate immune activation and help reveal whether an intervention reduces inflammatory signaling.
Researchers use LPS stimulation as a controlled model of innate immune activation. The experimental response can be examined through the resulting inflammatory signaling and cytokine production, including tumor necrosis factor and interleukins. This approach provides a defined way to investigate how immune cells respond to a bacterial component without relying exclusively on the complexity of a complete infection.
The model is useful when researchers need to test whether a treatment can reduce inflammation triggered through the CD14 and MD-2-TLR4 pathway. By comparing inflammatory signaling or cytokine production with and without treatment, investigators can assess anti-inflammatory activity. Results may also clarify which stages of innate immune activation are affected.
LPS-induced inflammation connects bacterial structure with host immune behavior, making it valuable for studying host-pathogen interaction. It helps researchers examine how recognition of Gram-negative bacterial components activates innate defenses and how excessive responses contribute to systemic inflammatory disease. The same framework supports investigation of infection mechanisms, inflammatory injury, and potential therapeutic strategies.