Titlebook: Neuro-Immuno-Gastroenterology; Cris Constantinescu,Razvan Arsenescu,Violeta Arsen Book 2016 Springer International Publishing Switzerland

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Microbial Regulation of Gastrointestinal Immunity in Health and Disease,upply from ingested food. The gastrointestinal immune system shapes the communities of microbes throughout the GI tract, and in turn, the microbiota provide metabolites and other cues to support the development and normal function of the immune system. Emerging research shows that this influence on

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Roles of Substance P in Gastrointestinal Functions and Neuroimmune Interactions,an systems and a number of functions also in the gastrointestinal (GI) tract. In the current chapter, the roles of SP and other TKs in the GI tract with wider implications and its role in intersystem communication are emphasized. Roles for SP and different neurokinin receptors in the enteric nervous

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Immunomodulation by Vasoactive Intestinal Polypeptide (VIP),ty of GI resident immune cells facilitates its immunoregulatory functions, including effects on macrophages, dendritic cells, and T lymphocytes. Here we discuss the functions of VIP as a modulator and possible therapeutic target in gastrointestinal inflammation in the larger context of its general i

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Stress and the Gastrointestinal System, related peptides urocortins (Ucns 1,2,3) are the mediators of stress. They are present both in the central nervous system and in the gastrointestinal (GI) tract where they exert their biological actions on target cells through activation of two receptors, CRF1 and CRF2. Stress is able to modulate n

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,Nutrition, Macrobiotics, and the Brain’s Neuroinflammatory Response, molecules can modulate the blood-brain barrier and immune cell traffic to the brain. Alteration in the brain cytokine milieu results in microglial polarization that dictates the outcome of inflammatory process. Preclinical and clinical studies have revealed the anti-inflammatory properties of plant

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,Guillain–Barré Syndrome and , Enteritis,tic to its history is an antecedent illness and this includes . enteritis. The pathogenesis of .-related Guillain–Barré syndrome has been extensively studied, and there is good evidence to support molecular mimicry between self and microbial components as the mechanism of disease. Self-antigens in t

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