Hormones as Immune Modulating Agents
Thomas F. Kresina in Immune Modulating Agents, 2020
Alpha-melanocyte stimulating hormone is produced by spleen cells and by keratinocytes and is present in the aqueous humour of the eye [150,180,181]. It has an inhibitory effect on thymocyte proliferation, neutrophilia, the production of acute-phase proteins by the liver, TNF and IFN-γ production, induction of prostaglandin E in fibroblasts, and contact sensitivity reactions. The immunosuppressive effect of IL-1β administered by the intracerebroventricular route could be blocked by the simultaneous infusion of α-MSH [182–189]. When administered to mice either systemically or locally at the site of treatment with contact sensitizing agents, α-MSH led to the induction of hapten-specific tolerance. Lymphocytes from regional lymph nodes of α-MSH treated mice failed to produce IL-2 5 days after sensitization. Tolerance induction by α-MSH could be abrogated in vivo by the administration of antibodies to IL-10 at the site of sensitization [190,191].
Melanocyte-Stimulating Hormone in the Central Nervous System
Mac E. Hadley in The Melanotropic Peptides, 1988
Alpha-melanocyte-stimulating hormone (α-MSH) was first described in neurons in the brain in 1978.1-3 The α-MSH immunoreactive material in the brain was later found to be comprised of both acetylated and desacetyl peptides, as occurs in the pituitary, but the brain contained relatively more of the desacetyl peptide.4-5 The distribution of α-MSH was remarkably similar to that previously shown for β-endorphin. This fact, combined with the discovery that α-MSH and β-endorphin were derived from a common prohormone, pro- opiomelanocortion (POMC), suggested the existence of a multiple neurotransmitter neuron for the first time.6,7 These findings have led to extensive studies of the POMC neuronal system and multiple neurotransmitters in the central nervous system.
Physiology of the Pituitary Gland
John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie in Basic Sciences Endocrine Surgery Rhinology, 2018
In addition, ACTH secretion has a superimposed pulsatile release pattern. The increase in cortisol is crucial for the appropriate stress response of the body and, if the hypothalamic–pituitary–adrenal (HPA) axis is compromised, cortisol treatment is life-saving in stress situations such as infection or surgery. Since ACTH is derived from POMC, conditions that lead to synthesis of large amounts of ACTH will also result in accumulation of other POMC-derived peptides. Raised levels of the alpha melanocyte-stimulating hormone lead to characteristic darkening of the skin. This phenomenon is seen in adrenal insufficiency, ectopic ACTH-secreting tumours and Nelson syndrome.
Melanocortin 5 Receptor Expression and Recovery of Ocular Immune Privilege after Uveitis
Published in Ocular Immunology and Inflammation, 2022
Tat Fong Ng, Ambika Manhapra, David Cluckey, Yoona Choe, Srujan Vajram, Andrew W. Taylor
The eye has adapted within its tissue microenvironment several mechanisms, which work to prevent and suppress the activation of inflammation that establishes immune privilege.1 The mechanisms of immune privilege are mediated in part by neuropeptides produced within the eye. These molecules mediate localized suppression of inflammation, prevent activation of effector T cells, and promote immune tolerance to antigen expressed within the eye. An essential mediator of these immunomodulating mechanisms is the neuropeptide alpha-melanocyte-stimulating hormone (α-MSH).1–3 The neuropeptide α-MSH is constitutively expressed within the eye, and retinal pigment epithelial cells (RPE) are a source of α-MSH.4,5 In the aqueous humor, α-MSH mediates aqueous humor suppression of effector T cell activation and induces T cell production of TGF-β that further suppresses immune cell activity.6 In the conditioned media of RPE-eyecups, α-MSH suppresses pro-inflammatory activity, promotes anti-inflammatory cytokine production, alters the maturation of phagosomes, and induces suppressor cell activity in macrophages.5,7–12
Skin impacts from exposure to ultraviolet, visible, infrared, and artificial lights – a review
Published in Journal of Cosmetic and Laser Therapy, 2021
Juliana Yuka Furukawa, Renata Miliani Martinez, Ana Lucía Morocho-Jácome, Thalía Selene Castillo-Gómez, Vecxi Judith Pereda-Contreras, Catarina Rosado, Maria Valéria Robles Velasco, André Rolim Baby
In parallel, there is regulation of skin pigmentation, through melanin, recognized by the skin tanning. The mechanism is divided into two phases: an initial rapid response of distribution and molecular changes in the existing melanin; hours or days after exposure, a delayed response occurs of melanin synthesis with subsequent transfer to keratinocytes. The process begins through hormonal interactions between keratinocytes and melanocytes – after damage caused to the DNA of keratinocytes, there is the production of a pro-opiomelanocortin gene, which stimulates the production and secretion of alpha-melanocyte-stimulating hormone. In this way, the skin is more protected against possible future exposures. Moreover, skin pigmentation depends on the type of skin, which is defined by the proportion of the main chemical structures of melanin: eumelanin and pheomelanin. Such proportion also defines the cutaneous response to UV radiation, as well as cancer risk (13).
Is there a therapeutic potential in combining bupropion and naltrexone in schizophrenia?
Published in Expert Review of Neurotherapeutics, 2022
Samer A. El Hayek, Malek A. Shatila, Jana A. Adnan, Luna E. Geagea, Firas Kobeissy, Farid R. Talih
BUPNAT is an oral extended-release tablet composed of a combination of the dopamine (DA) and norepinephrine (NE) reuptake inhibitor bupropion (BUP) and the µ-opioid receptor antagonist naltrexone (NAT) [18]. The BUP 90 mg/NAT 8 mg formulation (marketed under the brand name Contrave by Orexigen Therapeutics), is typically titrated to 4 tablets per day (BUP 360 mg/NAT 32 mg) by the fourth week of treatment [19]. The development of the drug started in the late 2000s. It gained FDA approval for the treatment of obesity in 2014 [20]. It is hypothesized to work via the stimulation of the hypothalamic pro-opiomelanocortin (POMC) neurons that release alpha-melanocyte-stimulating hormone (α-MSH). α-MSH, in turn, targets specific receptors that serve to reduce caloric intake and increase energy expenditure. When α-MSH is released, POMC neurons also simultaneously secrete µ-opioid receptor agonists. This activates a negative feedback loop on the system. BUPNAT works on both pathways by stimulating POMC neurons (via its BUP component) and inhibiting the negative feedback loop (through the NAT component) [21] (Figure 1).
Related Knowledge Centers
- Biological Pigment
- Chemical Structure
- Melanocortin
- Neuropeptide
- Peptide
- Peptide Hormone
- Melanocyte
- Protein Primary Structure
- Melanocyte-Stimulating Hormone
- Hair