Author Topic: Hypersensitivity Megathread  (Read 1616 times)

Muon

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Re: Hypersensitivity Megathread
« Reply #60 on: March 30, 2019, 09:44:53 AM »
Concept: Altered stress state/response(Neuroendocrine dysregulations)--->Immune function---->Delayed-type hypersensitivity?

Enhancing versus suppressive effects of stress hormones on skin immune function.

Abstract
Delayed-type hypersensitivity (DTH) reactions are antigen-specific cell-mediated immune responses that, depending on the antigen, mediate beneficial (e.g., resistance to viruses, bacteria, and fungi) or harmful (e.g., allergic dermatitis and autoimmunity) aspects of immune function. Contrary to the idea that stress suppresses immunity, we have reported that short-duration stressors significantly enhance skin DTH and that a stress-induced trafficking of leukocytes to the skin may mediate this immunoenhancement.

Here, we identify the hormonal mediators of a stress-induced enhancement of skin immunity. Adrenalectomy, which eliminates the glucocorticoid and epinephrine stress response, eliminated the stress-induced enhancement of skin DTH. Low-dose corticosterone or epinephrine administration significantly enhanced skin DTH and produced a significant increase in the number of T cells in lymph nodes draining the site of the DTH reaction. In contrast, high-dose corticosterone, chronic corticosterone, or low-dose dexamethasone administration significantly suppressed skin DTH.

These results suggest a role for adrenal stress hormones as endogenous immunoenhancing agents. These results also show that hormones released during an acute stress response may help prepare the immune system for potential challenges (e.g., wounding or infection) for which stress perception by the brain may serve as an early warning signal.

https://www.ncbi.nlm.nih.gov/pubmed/9927693

Is CRH worth investigating? (HPA/CRH hyperactivity?)

Brain-immune interactions and disease susceptibility



Schematic illustration of neural immune connections. The figure shows immune signaling of the CNS via systemic routes and the vagus nerve (Vagus n.) and CNS regulation of immunity via the hypothalamic-pituitary-adrenal (HPA), hypothalamic-pituitary-thyroid (HPT) and hypothalamic-pituitary-gonadal (HPG) axes, and the sympathetic nervous system (SNS) and parasympathetic nervous system (PNS). Cytokine expression within the CNS is represented by asterisks within the brain. Dotted lines represent negative regulatory pathways, and solid lines represent positive regulatory pathways. CRH, corticotrophin-releasing hormone; AVP, arginine vasopressin; TRH, thyrotropin-releasing hormone; GnRH, gonadotropin-releasing hormone; ACTH, adrenocorticotrophin hormone; TSH, thyroid-stimulating hormone; T4, thyroxine; T3, triiodothyronine; LH, luteinizing hormone; FSH, follicle-stimulating hormone; SNS, sympathetic nervous system; PNS, parasympathetic nervous system; LC, locus ceruleus; A1, C1, A2, C2, brainstem adrenergic nuclei.
« Last Edit: March 30, 2019, 12:58:58 PM by Muon »