REGULATION OF NEUTROPHIL MIGRATION TO INFLAMMATION
thesisposted on 10.06.2019 by Wenqing Zhou
In order to distinguish essays and pre-prints from academic theses, we have a separate category. These are often much longer text based documents than a paper.
Neutrophils, contributing to approximately 40%-70% of white blood cells in mammals, are the most abundant type of leukocytes in human circulation. As critical effector cells in innate immunity, neutrophils form the first line of host defense against microbes and are the first immune cells recruited to an inflamed tissue. The pathogen phagocytosis, release of reactive chemicals and proteases, and formation of extracellular traps are the key weapons of neutrophils in host defense. However, neutrophils also contribute to collateral tissue damage when performing their antimicrobial functions. The destructive potential of neutrophils requires the tight regulation of their activation and recruitment. In this study, we found that miR-223 in epithelial cells controls neutrophil response to inflammation through regulating the activation of NF-kB. As fast moving cells, neutrophils rely on glycolysis for energy production. The function of mitochondria in neutrophil motility is unknown. We demonstrated that mitochondria play an indispensable role in neutrophil migration: the biogenesis of mitochondria, mitochondrial ROS and the interaction between mitochondria and ER are all involved in maintaining the movement of neutrophils.