Related Experiment Video
Updated: May 27, 2026

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
The NOD-like receptor NLRP12 attenuates colon inflammation and tumorigenesis
Md Hasan Zaki1, Peter Vogel, R K Subbarao Malireddi
1Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Abstract:
NLRP12 is a member of the intracellular Nod-like receptor (NLR) family that has been suggested to downregulate the production of inflammatory cytokines, but its physiological role in regulating inflammation has not been characterized. We analyzed mice deficient in Nlrp12 to study its role in inflammatory diseases such as colitis and colorectal tumorigenesis. We show that Nlrp12-deficient mice are highly susceptible to colon inflammation and tumorigenesis, which is associated with increased production of inflammatory cytokines, chemokines, and tumorigenic factors. Enhanced colon inflammation and colorectal tumor development in Nlrp12-deficient mice are due to a failure to dampen NF-κB and ERK activation in macrophages. These results reveal a critical role for NLRP12 in maintaining intestinal homeostasis and providing protection against colorectal tumorigenesis.
Insights
NLRP12 (Nod-like receptor 12) normally suppresses inflammation. Mice lacking NLRP12 show increased susceptibility to colon inflammation and colorectal tumors due to unchecked inflammatory pathways.
Area of Science:
- Immunology
- Molecular Biology
- Gastroenterology
Background:
- The intracellular Nod-like receptor (NLR) family protein NLRP12 is implicated in regulating inflammatory cytokine production.
- The precise physiological role of NLRP12 in inflammation and associated diseases remains largely uncharacterized.
Purpose of the Study:
- To investigate the function of NLRP12 in inflammatory conditions, specifically focusing on colitis and colorectal tumorigenesis.
- To elucidate the molecular mechanisms by which NLRP12 influences inflammatory responses and tumor development.
Main Methods:
- Analysis of Nlrp12-deficient mice models.
- Assessment of inflammatory cytokine and chemokine production in the colon.
- Evaluation of NF-κB and ERK activation pathways in macrophages.
- Monitoring of colon inflammation and colorectal tumor development.
Main Results:
- Nlrp12-deficient mice exhibited heightened susceptibility to colon inflammation and colorectal tumorigenesis.
- Increased production of inflammatory cytokines, chemokines, and tumorigenic factors was observed in Nlrp12-deficient mice.
- Failure to dampen NF-κB and ERK activation in macrophages contributed to enhanced inflammation and tumor growth.
- NLRP12 deficiency led to a breakdown in intestinal homeostasis.
Conclusions:
- NLRP12 plays a critical role in maintaining intestinal homeostasis.
- NLRP12 acts as a crucial protector against the development of colorectal tumorigenesis.
- Targeting NLRP12 may offer therapeutic strategies for inflammatory bowel diseases and colorectal cancer.
More Related Videos
08:37Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
Published on: April 21, 2015
06:24Establishment of Coloproctitis Cancer Model in Mice and Evaluation of Therapeutic Effect of Chinese Medicine
Published on: October 13, 2023
Related Concept Videos
Role Of Notch Signalling In Intestinal Stem Cell Renewal
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
Inflammatory Bowel Disease II: Ulcerative Colitis
Inflammatory Bowel Disease III: Crohn's Disease