There is a functional communication between the gastrointestinal (GI) and central nervous system. This communication is bidirectional and it involves anatomic connections like the vagus nerve and humoral components including the immune system and the hypothalamus-pituitary-adrenal axis. There is increasing evidence suggesting that another key player in this interaction is the intestinal microbiota.1 Physical and psychological stress is known to affect not only the immune system, but also hormonal and GI homeostasis. Immune mechanisms are regulated by the hypothalamic-pituitary-adrenal axis as well as by neuronal influences through sympathetic, parasympathetic, and peptidergic/ sensory innervation of peripheral tissues. Immune and neuroendocrine systems have been shown to exert integrated responses to environmental signals and the relationship between stress and immune function has been demonstrated in many contexts, including proliferative response to mitogens and cellular activity.2 Stress conditions can lead to an imbalance between proinflammatory and anti-inflammatory cytokines or to an uncontrolled production of cytokines. Disregulation of innate and adaptive intestinal immune responses directed against the bacterial flora including a breakdown of oral tolerance to environmental antigens and commensals are involved in several pathogenetic mechanisms.3 Moreover, the integrity of intestinal ecosystem could be affected by several external factors, including antibiotic use, radiation, altered GI tract peristalsis, dietary changes, psychological, and physical stress. Studies conducted either in humans and in animal models demonstrated that psychological stress.

Stress and immune function : there is a role for the gut microbiota? / A. Castellazzi, S.C. Tagliacarne, S. Soldi, S. Perna, L. Ziviani, S. Milleri, L. Montagna, C. Valsecchi. - In: JOURNAL OF CLINICAL GASTROENTEROLOGY. - ISSN 0192-0790. - 52:suppl. 1(2018 Nov), pp. S66-S67. ((Intervento presentato al 9. convegno Probiotics, Prebiotics and New Foods, Nutraceuticals and Botanicals for Nutrition & Human and Microbiota Health Meeting tenutosi a Roma nel 2017 [10.1097/MCG.0000000000001056].

Stress and immune function : there is a role for the gut microbiota?

S. Perna;
2018

Abstract

There is a functional communication between the gastrointestinal (GI) and central nervous system. This communication is bidirectional and it involves anatomic connections like the vagus nerve and humoral components including the immune system and the hypothalamus-pituitary-adrenal axis. There is increasing evidence suggesting that another key player in this interaction is the intestinal microbiota.1 Physical and psychological stress is known to affect not only the immune system, but also hormonal and GI homeostasis. Immune mechanisms are regulated by the hypothalamic-pituitary-adrenal axis as well as by neuronal influences through sympathetic, parasympathetic, and peptidergic/ sensory innervation of peripheral tissues. Immune and neuroendocrine systems have been shown to exert integrated responses to environmental signals and the relationship between stress and immune function has been demonstrated in many contexts, including proliferative response to mitogens and cellular activity.2 Stress conditions can lead to an imbalance between proinflammatory and anti-inflammatory cytokines or to an uncontrolled production of cytokines. Disregulation of innate and adaptive intestinal immune responses directed against the bacterial flora including a breakdown of oral tolerance to environmental antigens and commensals are involved in several pathogenetic mechanisms.3 Moreover, the integrity of intestinal ecosystem could be affected by several external factors, including antibiotic use, radiation, altered GI tract peristalsis, dietary changes, psychological, and physical stress. Studies conducted either in humans and in animal models demonstrated that psychological stress.
gut-brain axis; immunity; microbiota; stress
Settore MED/49 - Scienze Tecniche Dietetiche Applicate
nov-2018
Article (author)
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/955782
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