Immunomodulacja: leczenie żywieniem – cz. II - Vetkompleksowo – serwis dla lekarzy weterynarii

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Immunomodulacja: leczenie żywieniem – cz. II

Immunonutrition– part II

At the molecular level, stress appears to delay inflammation by reducing efficiency of CD62L-mediated immune surveillance by phagocytes (Kehrli et al., 61-81). Stress decreases IFN-γ gamma secretion by lymphocytes, and may decrease antigen presentation efficiency by down-regulating MHC class II molecule expression on APCs, and delay or impair immune responses to vaccination.

Stress sets into motion physiological changes that help the organism cope with the stressor – fight or flight response. However, chronic stress results in sustained activation of stress responses, which include the activation of the hypothalamic-pituitary-adrenal axis and the sympathetic-adrenal-medullary axis, resulting in the production of glucocorticoid (GC) hormones and catecholamine. GC receptors are expressed by a variety of immune cells and they bind cortisol, interfering with NF-κB function, which in turn regulates the activity of cytokine-producing immune cells. Sustained release of stress hormones negatively impacts the immune system. Several models have been proposed to explain the mechanism of action of stress hormones in the immune cells (Padgett and Glaser, 444-48).

GC impact the expression of cytokines, co-stimulatory molecules and adhesion molecules which influences the immune cell migration, differentiation, proliferation and effector function (Mirani et al., 6361-68; Ashwell, Vacchio, and Galon, 644-46; Russo-Marie, 281-86). Adrenergic receptors bind epinephrine and norepinephrine and activate the cAMP response element binding protein, inducing the transcription of genes encoding a variety immune response gene including genes for cytokines. [...]

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