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Free keywords:
skin microbiota, inflammatory skin disease, bullous pemphigoid, anorexia nervosa, nell2 gene
Abstract:
The skin is the largest organ in the human body, approximately 1.5 to 2 m2 in area, and serves as a crucial physical and immune barrier from our environment. Yet, the skin is home to billions of microorganisms inhabiting a multitude of folds, invaginations, and specialized niches that sustain microscopic life (Grice and Segre, 2011; Scharschmidt and Fischbach, 2013). We are not teeming with bugs so much as we are irrevocably intertwined with microbiota such that, throughout evolutionary history, these bacteria, fungi, and viruses have become invaluable parts of our physiology, cooperatively acting as a hidden organ. The microbiota colonizing the skin, their genetic material, and their microenvironments are collectively referred to as the skin microbiome (Marchesi and Ravel, 2015). Most microorganisms are not pathogens. Rather, the majority of microorganisms living on their hosts are benign and, in some cases, beneficial, performing functions vital for host physiology and homeostasis. Scientists are beginning to unravel how the skin microbiome is interfacing with different physiological processes of the mammalian host. Microbiota living on us, but also residing within deeper layers of the skin, contribute to host inflammation, epidermal barrier function, and immunity through feedback mechanisms with our immune cells (Grice and Segre, 2011). Microbiota even contribute to host defense through the production of bactericidal factors (Iacob et al., 2018; Jacobs et al., 2017; Nakatsuji et al., 2017; Zheng et al., 2020). Microbiome researchers are interested in understanding these mechanisms that link commensal microbes with host biology and how these interactions contribute to host health or disease. This thesis aims to characterize resident skin microbiota communities the context of inflammatory cutaneous disease.
