: Oxidized low-density lipoprotein (ox-LDL) is a proinflammatory particle associated with various diseases and affects cell proliferation and viability in multiple cell types. However, its impact on intestinal epithelial cells remains underexplored. This study investigates the effect of ox-LDL on colonic epithelial cell proliferation and viability, as well as the underlying mechanisms involved.
View Article and Find Full Text PDFCancer immunotherapy has become an indispensable mode of treatment for a multitude of solid tumor cancers. Colorectal cancer (CRC) has been one of the many cancer types to benefit from immunotherapy, especially in advanced disease where standard treatment fails to prevent recurrence or results in poor survival. The efficacy of immunotherapy in CRC has not been without challenge, as early clinical trials observed dismal responses in unselected CRC patients treated with checkpoint inhibitors.
View Article and Find Full Text PDFCell Mol Gastroenterol Hepatol
September 2023
Background & Aims: Metabolic syndrome (MetS) is characterized by obesity, glucose intolerance, and hepatic steatosis. Alterations in the gut microbiome play important roles in the development of MetS. However, the mechanisms by which this occurs are poorly understood.
View Article and Find Full Text PDFBackground & Aims: Chronic colonic inflammation leads to dysplasia and cancer in patients with inflammatory bowel disease. We have described the critical role of innate immune signaling via Toll-like receptor 4 (TLR4) in the pathogenesis of dysplasia and cancer. In the current study, we interrogate the intersection of TLR4 signaling, epithelial redox activity, and the microbiota in colitis-associated neoplasia.
View Article and Find Full Text PDFBackground: Patients with inflammatory bowel disease (IBD) have intestinal inflammation and are treated with immune-modulating medications. In the face of the coronavirus disease-19 pandemic, we do not know whether patients with IBD will be more susceptible to infection or disease. We hypothesized that the viral entry molecules angiotensin I converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2) are expressed in the intestine.
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