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13 results on '"Webster, Nicole L."'

11. Multi-transgenic pigs expressing three fluorescent proteins produced with high efficiency by sperm mediated gene transfer

Author

Webster, Nicole L., primary, Forni, Monica, additional, Bacci, Maria Laura, additional, Giovannoni, Roberto, additional, Razzini, Riccardo, additional, Fantinati, Paolo, additional, Zannoni, Augusta, additional, Fusetti, Lisa, additional, Dalprà, Leda, additional, Bianco, Maria Rosaria, additional, Papa, Michele, additional, Seren, Eraldo, additional, Sandrin, Mauro S., additional, Mc Kenzie, Ian F.C., additional, and Lavitrano, Marialuisa, additional

Published
2005
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12. Phagocytosis stimulates mobilization and shedding of intracellular CD16A in human monocytes and macrophages: inhibition by HIV‐1 infection

Author

Webster, Nicole L., Kedzierska, Katherine, Azzam, Rula, Paukovics, Geza, Wilson, John, Crowe, Suzanne M., and Jaworowski, Anthony

Abstract

Surface and intracellular staining coupled with flow cytometric analysis was used to show for the first time that human macrophages and a minor subset of peripheral blood monocytes have an internal pool of CD16A, which is mobilized and shed during Fc receptor for immunoglobulin G‐mediated phagocytosis. Human immunodeficiency virus type 1 (HIV‐1) infection of monocyte‐derived macrophages in vitro led to a reduction in the phagocytosis‐induced up‐regulation in CD16A shedding. These results suggest that monocytes and macrophages may be a source of soluble CD16A, which is elevated in the serum of patients in a variety of disease states and that the mobilization and shedding of CD16A in response to phagocytosis are disrupted by HIV‐1 infection.

Published
2006
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13. Kynurenine pathway metabolism in human blood-brain-barrier cells: implications for immune tolerance and neurotoxicity.

Author

Owe-Young R, Webster NL, Mukhtar M, Pomerantz RJ, Smythe G, Walker D, Armati PJ, Crowe SM, and Brew BJ

Subjects
Blood-Brain Barrier immunology, Blood-Brain Barrier pathology, Cells, Cultured, Endothelial Cells immunology, Endothelial Cells metabolism, Endothelial Cells pathology, Humans, Kynurenine genetics, Kynurenine metabolism, Neurotoxicity Syndromes genetics, Neurotoxicity Syndromes pathology, Pericytes immunology, Pericytes metabolism, Pericytes pathology, Blood-Brain Barrier metabolism, Immune Tolerance, Kynurenine physiology, Neurotoxicity Syndromes metabolism, Signal Transduction immunology
Abstract

The catabolic pathway of l-tryptophan (l-trp), known as the kynurenine pathway (KP), has been implicated in the pathogenesis of a wide range of brain diseases through its ability to lead to immune tolerance and neurotoxicity. As endothelial cells (ECs) and pericytes of the blood-brain-barrier (BBB) are among the first brain-associated cells that a blood-borne pathogen would encounter, we sought to determine their expression of the KP. Using RT-PCR and HPLC/GC-MS, we show that BBB ECs and pericytes constitutively express components of the KP. BBB ECs constitutively synthesized kynurenic acid, and after immune activation, kynurenine (KYN), which is secreted basolaterally. BBB pericytes produced small amounts of picolinic acid and after immune activation, KYN. These results have significant implications for the pathogenesis of inflammatory brain diseases in general, particularly human immunodeficiency virus (HIV)-related brain disease. Kynurenine pathway activation at the BBB results in local immune tolerance and neurotoxicity: the basolateral secretion of excess KYN can be further metabolized by perivascular macrophages and microglia with synthesis of quinolinic acid. The results point to a mechanism whereby a systemic inflammatory signal can be transduced across an intact BBB to cause local neurotoxicity.

Published
2008
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