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How do the brain and the immune system interact, and what are the consequences of this interaction on the physiology of an organism during infection? The main focus of my thesis is neuroimmune interaction, as studied in the following: (1) circadian regulation of immune system function, specifically phagocytosis by immune cells during bacterial infection; (2) the impact of circadian-regulated metabolism and feeding behavior on immunity and host tolerance of bacterial infection; and (3) immune system function in the context of Fragile X syndrome, a neurological disease known to cause circadian dysregulation. To investigate the interactions between these complex physiologies, I use the well-characterized and genetically tractable Drosophila melanogaster animal model. Each topic is briefly introduced in Chapter 1. Chapter 2 focuses on the body of work identifying the circadian regulation of the immune system, particularly phagocytosis, by immune cells during bacterial infection. Chapter 3 highlights findings regarding how diet and host metabolic state impact survival after infection. Chapter 4 illustrates phagocytic immune cell defects both systemically and in the brain in the Drosophila model of Fragile X syndrome. Lastly the conclusions discuss how these three works have built on our fund of knowledge of neuroimmune interactions and the future implications for these results.

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