In Stock Cell Lines
The NLRP6 Knockout IPEC-J2 Cell Line is a CRISPR/Cas9-edited porcine intestinal epithelial cell line with a targeted loss-of-function mutation in the NLRP6 gene. NLRP6 is an innate immune sensor that forms an inflammasome with ASC and caspase-1 to drive secretion of IL-18 and IL-1??, while also regulating NF-??B signaling and antimicrobial peptide production, thereby maintaining intestinal homeostasis and shaping the gut microbiota. This knockout cell line enables investigation of inflammasome signaling, epithelial barrier function, and host-microbe interactions in contexts such as inflammatory bowel disease and viral gastroenteritis. Supported assays include transepithelial electrical resistance, ELISA for IL-18/IL-1??, and ASC speck imaging, facilitating preclinical therapeutic studies.
The NLRP6 Knockout IPEC-J2 Cell Line is a CRISPR/Cas9-mediated gene-disrupted cell line derived from the porcine jejunal epithelial line IPEC-J2, providing a stable loss-of-function model for investigating NLRP6-dependent processes in intestinal epithelial cells. By eliminating NLRP6 expression, this cell line facilitates mechanistic studies of inflammasome biology and epithelial innate immune signaling without off-target pharmacological effects. This engineered knockout serves as a precise tool for dissecting the role of NLRP6 in mucosal defense, barrier maintenance, and host-microbe crosstalk.
IPEC-J2 is a non-transformed, continuous intestinal epithelial cell line isolated from porcine jejunum, retaining key characteristics of primary epithelial cells such as polarized monolayer formation, tight junction integrity, nutrient transport, and innate immune responsiveness. The preserved epithelial phenotype ensures that knockout phenotypes reflect endogenous signaling events in a physiologically relevant context. It recapitulates critical features of the intestinal barrier, making it a well-established model for porcine and translational research on epithelial permeability, host-pathogen interactions, and inflammatory pathways relevant to human gastrointestinal diseases.
NLRP6 is a cytosolic innate immune sensor responding to microbial ligands (muramyl dipeptide, LPS), viral RNA, type I interferons, IL-18, and gut microbiota metabolites. Upon activation, NLRP6 oligomerizes and assembles a multiprotein inflammasome with the adaptor ASC (PYCARD) and pro-caspase-1, leading to autocatalytic activation of caspase-1 and subsequent cleavage of pro-IL-18 and pro-IL-1?? into their mature secreted forms. This complex can also induce gasdermin D-dependent pyroptosis. Beyond inflammasome formation, NLRP6 negatively regulates NF-??B signaling and interacts with MAVS, DHX15, and the putative E3 ubiquitin ligase TRIM31. Downstream, NLRP6 activity modulates expression of antimicrobial peptides such as ??-defensins, thereby influencing mucosal innate defense and gut microbiota composition.
In intestinal epithelial cells, NLRP6-mediated cytokine release, particularly IL-18 and IL-1??, is critical for maintaining mucosal barrier integrity and regulating intestinal homeostasis. The IPEC-J2 knockout model uniquely enables dissection of epithelial-intrinsic NLRP6 functions in barrier formation, innate defense, and homeostatic signaling, independent of immune cell contributions. This system is directly relevant to studying the molecular pathogenesis of inflammatory bowel disease, colitis, colorectal cancer, viral gastroenteritis, and metabolic syndrome, where dysregulated NLRP6 signaling is implicated in disrupted epithelial homeostasis and aberrant host-microbe interactions.
Researchers can employ this knockout line for western blotting and RT-qPCR validation of inflammasome components, ELISA quantification of secreted IL-18 and IL-1??, caspase-1 activity assays, and immunofluorescence imaging of ASC specks. Functional studies of barrier integrity using transepithelial electrical resistance (TEER) and microbial challenge assays enable investigation of host-microbe interactions. These applications support preclinical research into mucosal immunity and anti-inflammatory therapies targeting NLRP6 pathways. For further information, please contact Ascent Research.
