| Quantity: | |
|---|---|
Complementary mechanisms – MSU model mimics crystal-induced inflammation (gout-related); LPS model mimics bacterial endotoxin-induced inflammation.
Quantifiable endpoints – Neutrophil counts in peritoneal lavage fluid (MSU model), IL-1β and IL-6 levels in peritoneal lavage fluid and blood (LPS model).
Rapid and reproducible – Both models induce acute inflammation within hours, allowing rapid screening of anti-inflammatory compounds.
Translational value – Ideal for testing anti-inflammatory drugs (NSAIDs, corticosteroids), IL-1 inhibitors (anakinra, canakinumab), and TLR4 antagonists.
IND-ready data packages – Studies can be conducted in accordance with GLP principles.
MSU Induced C57BL/6 Peritonitis Model
LPS Induced C57BL/6 Peritonitis Model
• Efficacy testing of anti-inflammatory drugs (NSAIDs, corticosteroids, COX-2 inhibitors)
• Evaluation of IL-1 inhibitors (anakinra, canakinumab), NLRP3 inflammasome inhibitors, and TLR4 antagonists
• Target validation for neutrophil recruitment and cytokine pathways
• Biomarker discovery (neutrophil markers, cytokine signatures)
• IND-enabling pharmacology and toxicology studies
Parameter | MSU Induced Peritonitis Model | LPS Induced Peritonitis Model |
Species/Strain | C57BL/6 mouse | C57BL/6 mouse |
Induction method | Intraperitoneal injection of MSU crystals (1–3 mg/mouse) | Intraperitoneal injection of LPS (5–20 mg/kg) |
Study duration | 4–24 hours post-induction | 2–24 hours post-induction |
Key endpoints | Neutrophil counts in peritoneal lavage fluid (flow cytometry or cytospin) | IL-1β and IL-6 levels in peritoneal lavage fluid and blood (ELISA) |
| Positive control | Dexamethasone or indomethacin available as reference anti-inflammatory compounds | |
| Data package | Raw data, analysis reports, cell counts, ELISA results, bioinformatics (optional)Raw data, analysis reports, cell counts, ELISA results, bioinformatics (optional) | |
Q: What are the differences between the MSU and LPS peritonitis models?
A: MSU crystals activate the NLRP3 inflammasome, leading to IL-1β-mediated neutrophilic inflammation, mimicking crystal-induced peritonitis (e.g., gout). LPS activates TLR4 signaling, triggering a broad pro-inflammatory cytokine response (IL-1β, IL-6, TNF-α), mimicking bacterial endotoxin-induced peritonitis.
Q: Which model is more suitable for testing NLRP3 inhibitors?
A: The MSU induced peritonitis model is specifically driven by NLRP3 inflammasome activation and IL-1β, making it ideal for evaluating NLRP3 inhibitors and IL-1 targeting therapies. The LPS model activates multiple pathways and is suitable for broader anti-inflammatory screening.
Q: Can these models be used for IND-enabling studies?
A: Yes. Studies can be conducted in accordance with GLP principles for regulatory submissions (FDA, EMA).
Q: Do you offer customized study protocols (e.g., different MSU doses, LPS concentrations, treatment timing)?
A: Absolutely. Our scientific team tailors induction protocols, treatment schedules (prophylactic or therapeutic), and endpoint analyses to your specific drug candidate.
Q: What is the typical timeline for a pilot efficacy study?
A: Both models are acute, with studies typically completed within 24 hours post-induction, allowing rapid screening of anti-inflammatory compounds.
