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Nordin M J Hanssen, Kristiaan Wouters, Maya S Huijberts, Marion J Gijbels, Judith C Sluimer, Jean L J M Scheijen, Sylvia Heeneman, Erik A L Biessen, Mat J A P Daemen, Michael Brownlee, Dominique P de Kleijn, Coen D A Stehouwer, Gerard Pasterkamp, Casper G Schalkwijk
AIMS: Rupture-prone atherosclerotic plaques are characterized by inflammation and a large necrotic core. Inflammation is linked to high metabolic activity. Advanced glycation endproducts (AGEs) and their major precursor methylglyoxal are formed during high metabolic activity and can have detrimental effects on cellular function and may induce cell death. Therefore, we investigated whether plaque AGEs are increased in human carotid rupture-prone plaques and are associated with plaque inflammation and necrotic core formation...
May 2014: European Heart Journal
Ulrike Steinmann, Julia Borkowski, Hartwig Wolburg, Birgit Schröppel, Peter Findeisen, Christel Weiss, Hiroshi Ishikawa, Christian Schwerk, Horst Schroten, Tobias Tenenbaum
BACKGROUND: Bacterial invasion through the blood-cerebrospinal fluid barrier (BCSFB) during bacterial meningitis causes secretion of proinflammatory cytokines/chemokines followed by the recruitment of leukocytes into the CNS. In this study, we analyzed the cellular and molecular mechanisms of polymorphonuclear neutrophil (PMN) and monocyte transepithelial transmigration (TM) across the BCSFB after bacterial infection. METHODS: Using an inverted transwell filter system of human choroid plexus papilloma cells (HIBCPP), we studied leukocyte TM rates, the migration route by immunofluorescence, transmission electron microscopy and focused ion beam/scanning electron microscopy, the secretion of cytokines/chemokines by cytokine bead array and posttranslational modification of the signal regulatory protein (SIRP) α via western blot...
2013: Journal of Neuroinflammation
Jennifer L Strande, Kasi V Routhu, Anna Hsu, Alfred C Nicolosi, John E Baker
BACKGROUND: The lanthanide cation, gadolinium (GdCl3) protects the myocardium against infarction following ischemia and reperfusion. Neutrophils and macrophages are the main leukocytes responsible for infarct expansion after reperfusion. GdCl3 interferes with macrophage and neutrophil function in the liver by decreasing macrophage secretion of inflammatory cytokines and neutrophil infiltration. We hypothesized that GdCl3 protects against ischemia and reperfusion injury by decreasing inflammation...
2009: Journal of Inflammation
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