Publications by authors named "Cody Kempen"
The interleukin (IL)-22 cytokine can be protective or inflammatory in the intestine. It is unclear if IL-22 receptor (IL-22Ra1)-mediated protection involves a specific type of intestinal epithelial cell (IEC). By using a range of IEC type-specific Il22Ra1 conditional knockout mice and a dextran sulfate sodium (DSS) colitis model, we demonstrate that IL-22Ra1 signaling in MATH1 cells (goblet and progenitor cells) is essential for maintaining the mucosal barrier and intestinal tissue regeneration.
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- IL-22 plays a crucial role in reducing metabolism issues caused by obesity, but its specific action sites are unclear.
- Researchers created mice with specific IL-22RA1 knockouts in the intestine, liver, and white adipose tissue to study its effects on metabolism when on a high-fat diet.
- Findings reveal that IL-22RA1 signaling in the intestine and liver improves glucose metabolism and influences fat tissue metabolism, highlighting the significance of gut signaling in managing obesity-related metabolic disorders.
Background/aims: The ribosome-inactivating proteins include the biothreat agent, ricin toxin (RT). When inhaled, RT causes near complete destruction of the lung epithelium coincident with a proinflammatory response that includes TNF family cytokines, which are death-inducing ligands. We previously demonstrated that the combination of RT and TNF-related apoptosis inducing ligand (TRAIL) induces caspase-dependent apoptosis, while RT and TNF-α or RT and Fas ligand (FasL) induces cathepsin-dependent cell death in lung epithelial cells.
View Article and Find Full Text PDFThe Th17 cell-lineage-defining cytokine IL-17A contributes to host defense and inflammatory disease by coordinating multicellular immune responses. The IL-17 receptor (IL-17RA) is expressed by diverse intestinal cell types, and therapies targeting IL-17A induce adverse intestinal events, suggesting additional tissue-specific functions. Here, we used multiple conditional deletion models to identify a role for IL-17A in secretory epithelial cell differentiation in the gut.
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- Previous research highlights the role of IL-17A in regulating gut microbiota and overall metabolic functions, but the specific site of IL-17RA signaling has not been explored.
- Using specific mouse models that lack IL-17RA in either the intestines or liver, the study found that gut IL-17RA signaling is crucial for managing metabolic functions when exposed to a high-fat diet.
- Mice lacking intestinal IL-17RA exhibited negative effects like poor glucose metabolism, abnormal hormone levels, increased body fat, and greater liver fat accumulation, linking changes in gut microbiota to systemic glucose regulation.
Article Synopsis
- IL-22 signaling plays a vital role in protecting the intestines, yet identifying the specific cell types that respond to it has been challenging due to the receptor’s expression across various cells.
- Research indicates that IL-22 signaling is linked with the differentiation of Paneth cells, important components of intestinal defense, rather than intestinal stem cells.
- The study reveals that IL-22 functions within Paneth cells to enhance their maturation, antimicrobial abilities, and interaction with gut microbiota, crucial for fighting off pathogens like Salmonella.
Ricin is a member of the ribosome-inactivating protein (RIP) family of toxins and is classified as a biothreat agent by the Centers for Disease Control and Prevention (CDC). Inhalation, the most potent route of toxicity, triggers an acute respiratory distress-like syndrome that coincides with near complete destruction of the lung epithelium. We previously demonstrated that the TNF-related apoptosis-inducing ligand (TRAIL; CD253) sensitizes human lung epithelial cells to ricin-induced death.
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