Impaired phagocytosis and chemotaxis of neutrophil by diabetes and superoxide deficiency
Date
2011
DOI
Authors
Kim, Bolam
Version
OA Version
Citation
Abstract
Diabetes mellitus is a group of diseases characterized by chronic hyperglycemia and other metabolic abnormalities that are due to insulin deficiency or defective insulin utilization. Several complications are caused by chronic hyperglycemia in diabetes mellitus. Neutrophil is the first line of host defense of the innate immune system, when there is infection or injury, they can be easily mobilized to the invading or injurious site where they localize invading microorganisms, and clear dead host cells and debris. The mode of action of neutrophils to the invading microorganism is (a) adhesion and migration: (b) phagocytosis and degranulation (C) apoptosis. In this study we investigated whether diabetes and superoxide deficiency impair phagocytosis and chemotaxis of neutrophils. We have tested neutrophils from wild type, Akita, Ncf1 and Akita/Ncf1 double mutant mice, representing normal, diabetic, superoxide deficient and diabetic/superoxide deficient models, respectively. Glucose level was measured from tail vein blood. Akita and Akita/Ncf1 showed markedly higher glucose level compared to WT and Ncf1. Flow cytometry showed marked increase in phagocytosis in Ncf1 neutrophils compared to all other models. The experiment of chemotactic activity measured by flow cytometry also showed remarkable result. Akita/Ncf1 model showed less chemotactic activity, but as time passed the gaps between two models are increased at each time point.
Description
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Thesis (MSD) --Boston University, Henry M. Goldman School of Dental Medicine, 2011 (Department of Oral Biology and Periodontology).
Includes bibliographic references: leaves 41-46.
Thesis (MSD) --Boston University, Henry M. Goldman School of Dental Medicine, 2011 (Department of Oral Biology and Periodontology).
Includes bibliographic references: leaves 41-46.
License
This work is protected by copyright. Downloading is restricted to the BU community. If you are the author of this work and would like to make it publicly available, please contact open-help@bu.edu.