Articles tagged with Intestinal Epithelium
Researchers at Cold Spring Harbor Laboratory have devised a new approach to stimulate cell growth and repair in the intestine using CAR T-cell therapy. This therapy has shown promising results in improving gut health in both young and old mice, with significant reductions in inflammation and improved nutrient absorption.
Cells on the intestinal surface are replaced every few days due to pulling forces that determine which cells are weakest and need to leave. Weakened cells are removed from the intestine due to disrupted tug-of-war behavior, leading to inflammation and disease.
A new cell type has been identified in Burmese pythons that produces large particles made from calcium, phosphorus, and iron to digest bones. This specialized cell type helps limit excessive calcium absorption and is found in multiple python and boa species as well as the Gila monster.
Scientists at IBEC create a system to control formation of intestinal crypts and villi using protein printing technique, enabling controlled analysis of gut biology. The method allows for detailed study of cell regeneration and diseases such as cancer and inflammatory diseases.
Researchers at TUM found that mitochondrial dysfunction in mice leads to chronic intestinal inflammation and changes in the gut microbiome. The study suggests potential new treatments targeting mitochondrial pathways or addressing the connections between the microbiome and mitochondria.
Researchers from the Hubrecht Institute found that tuft cells can proliferate and generate new epithelial cell types, restoring damaged gut tissue. This discovery may have important implications for regenerative medicine.
Neotame has been shown to cause previously healthy gut bacteria to become diseased and invade the gut wall, potentially leading to irritable bowel syndrome and sepsis. The study also found a breakdown of the epithelial barrier, which forms part of the gut wall.
Researchers used gut organoids to study gut cell differentiation, identifying ZNF800 as a key regulator of enteroendocrine cells. The discovery could have implications for understanding gastrointestinal diseases and endocrine disorders.
Researchers at UC Riverside have discovered a new cell type in the thymus that is similar to M cells found in the gut and airways. The newly discovered cells are like gatekeepers, acting as antigen-delivery cells for the immune system in organs such as the intestine and lung.
A UC Riverside-led study found that reduced PTPN2 activity in intestinal epithelial cells leads to decreased Paneth cell antimicrobial peptide production, disrupting the gut microbiota and increasing E. coli. This loss can serve as a marker of IBD disease.
Research reveals that lymphatic capillaries communicate with intestinal stem cells to regulate their activity and promote regeneration. The findings provide new insights into the role of lymphatics in maintaining the health of the intestine.
A UC Riverside-led study identifies how loss-of-function mutations in the gene PTPN2 affect intestinal epithelial cells' ability to maintain a barrier. The researchers found that increased fluid loss and diarrhea are linked to the mutation, which can be reversed by treating cells with synthetic matriptase.
The human intestine constantly regenerates itself, with 10 billion epithelial cells replaced each day. Researchers have identified the stem-cell niche responsible for providing the activating signal to these stem cells, called Gli1-positive cells surrounding crypts.
A Johns Hopkins study of mice with metabolic syndrome found that the intestinal microbiome plays a substantial role in the development of obesity and insulin resistance. The research suggests that manipulating gut bacteria may prevent obesity and diabetes.
Researchers at Albert Einstein College of Medicine found that certain bacteria produce metabolites that strengthen the intestinal epithelium's barrier function. These metabolites activate a protein called PXR, which suppresses inflammatory responses and increases junction strength between epithelial cells.
The study reveals that EphB-ephrin bindings activate metaloprotease ADAM10, destroying binding between distinct cell types and preventing cell mixing. This mechanism is crucial for maintaining tissue organization in the intestinal epithelium.