Cytokines and Hypothalamo-Pituitary-Adrenal Axis Activation: Now a Classic of Immune-Neuroendocrine System Interactions
Résumé
Precise descriptions of neuroendrocrine and immune systems along with a more integrative orientation of research in the life sciences created the conditions in the last quarter of the 20th century to envision interactions between these systems. In particular, it was shown that pro-inflammatory cytokines, such as interleukin-1, produced in response to host detection of bacterial fragments, can activate the hypothalamo-pituitary-adrenal axis, resulting in the release of corticosteroids, which, in turn, have anti-inflammatory effects. Given the existence of the blood-brain barrier that prevents hydrophilic molecules like cytokines to passively enter the brain parenchyma, research efforts have focused on elucidating so-called cytokine-to-brain signaling pathways. The findings obtained indicate that several mechanisms, including prostaglandin-induced neuronal activation, vagal afferents and ascending catecholaminergic brainstem projections, can be involved in hypothalamo-pituitary-adrenal axis activation after systemic interleukin-1 administration depending on, both experimental and physiological, conditions. Most recently, both homeostatic-physiological stressors and emotionalpsychological stressors have been proposed to give rise to inflammatory responses suggesting that crosstalk between innate immune mediators and hypothalamo-pituitary-adrenal axis hormones will continue to be at the forefront of research.
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