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| http://dx.doi.org/10.1155/2015/765303 | DOI Listing |
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Brd4 modulates metabolic endotoxemia-induced inflammation by regulating colonic macrophage infiltration in high-fat diet-fed mice.
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Fujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases, Institute for Basic Medical Sciences, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
High-fat diet (HFD) induces low-grade chronic inflammation, contributing to obesity and insulin resistance. However, the precise mechanisms triggering obesity-associated metabolic inflammation remain elusive. In this study, we identified epigenetic factor Brd4 as a key player in this process by regulating the expression of Ccr2/Ccr5 in colonic macrophage.
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School of Public Health, Lanzhou University, Lanzhou, 730000, China.
The high-altitude, low-pressure, and hypoxia environment poses a significant threat to human health, particularly causing intestinal damage and disrupting gut microbiota. This study investigates the protective effects of Brassica rapa L. crude polysaccharides (BRP) on intestinal damage in mice exposed to hypobaric hypoxic conditions.
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Department of Microbiology and Immunology, Virginia Commonwealth University and Richmond VA Medical Center, Richmond, Virginia; Stravitz-Sanyal Institute for Liver Disease and Metabolic Health, School of Medicine, Virginia Commonwealth University, Richmond, Virginia. Electronic address:
Cholangiocarcinoma (CCA) is a rare but highly malignant carcinoma of bile duct epithelial cells with a poor prognosis. The major risk factors of CCA carcinogenesis and progression are cholestatic liver diseases. The key feature of primary sclerosing cholangitis and primary biliary cholangitis is chronic cholestasis, which means a slowdown of hepatocyte secretion of biliary lipids and metabolites into bile as well as a slowdown of enterohepatic circulation (bile acid recirculation) of bile acids with dysbiosis of the gut microbiome, which was shown to lead to enterohepatic recirculation and an increase of toxic secondary bile acids.
View Article and Find Full Text PDFSodium butyrate prevents lipopolysaccharide induced inflammation and restores the expression of tight junction protein in human epithelial Caco-2 cells.
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Defence Institute of Physiology and Allied Sciences, Delhi 110054, India. Electronic address:
The gastrointestinal (GI) tract is susceptible to damage under high altitude hypoxic conditions, leading to gastrointestinal discomfort and intestinal barrier injury. Sodium butyrate, a short-chain fatty acid present as a metabolite in the gut, has emerged as a promising therapeutic agent due to its ability to act as an immunomodulatory agent and restore intestinal barrier integrity. This study aimed to explore the mechanism by which sodium butyrate exhibits anti inflammatory effect on intestinal epithelial cells.
View Article and Find Full Text PDFImpact of Mast Cell Activation on Neurodegeneration: A Potential Role for Gut-Brain Axis and Infection.
Neurol Int
December 2024
Second Medical Clinic, School of Medicine, Ippokration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Greece.
Background: The innate immune response aims to prevent pathogens from entering the organism and/or to facilitate pathogen clearance. Innate immune cells, such as macrophages, mast cells (MCs), natural killer cells and neutrophils, bear pattern recognition receptors and are thus able to recognize common molecular patterns, such as pathogen-associated molecular patterns (PAMPs), and damage-associated molecular patterns (DAMPs), the later occurring in the context of neuroinflammation. An inflammatory component in the pathology of otherwise "primary cerebrovascular and neurodegenerative" disease has recently been recognized and targeted as a means of therapeutic intervention.
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