Plasma concentrations and anti-L-cytokine effects of α-melanocyte stimulating hormone in septic patients

Abstract

In patients with systemic inflammation, there are substantial changes over time in plasma concentrations of alpha-MSH that are reduced in early phases of the disease. Reduction of this endogenous modulator of inflammation could be detrimental to the host. Addition of alpha-MSH to LPS-stimulated blood samples reduces production of cytokines involved in development of septic syndrome. This inhibition by alpha-MSH, a peptide that is beneficial in treatment of experimental models of sepsis, might therefore be useful to treat sepsis syndrome in humans.

Central Neurotranspeptide, Alpha-Melanocyte-Stimulating Hormone (.ALPHA.-MSH) is Upregulated in Patients with Congestive Heart Failure

“…In human diseases, the relationship between concentrations of α-MSH and disease progression in HIV-infection was explored in a prospective study (19). Circulating α-MSH returned to normal levels in patients with sepsis syndrome who recovered and it remained low in those who died (20) As previously reported (23,24), the response to α-MSH was biphasic in inhibitory effects on LPS-induced TNF-α production. One of the possibilities of the reason may be that α-MSH could modulate both inflammatory and antiinflammatory responses regulating intracellular peroxide levels and glutathione peroxidase activity, and an excess dose of α-MSH could break the immunobalance (23).…”

α-MSH: A Potential Neuroprotective and Immunomodulatory Agent for the Treatment of Stroke

“…In a clinical study of patients with brain injury (either traumatic or resulting from subarachnoid hemorrhage), however, systemic decreases in a-MSH were documented; furthermore, lower concentrations of a-MSH were associated with worse neurologic outcomes (Magnoni et al, 2003). Similar decreases in circulating a-MSH were observed in critically ill patients without neurologic injury (Catania et al, 2000;Todd et al, 2009). Secretion of a-MSH from the pars intermedia is under hypothalamic control; release is tonically inhibited by dopamine and g-amino butyric acid (Saland, 2001).…”

Monitoring Immune Dysfunctions in the Septic Patient: A New Skin for the Old Ceremony

“…Many other mediators are known to be elevated during septic shock and to possess immunosuppressive properties; we can mention soluble HLA-G molecules, prostaglandin E2, α-melanocytestimulating hormone, adrenomedullin, and vaso-intestinal peptide (63)(64)(65)(66)(67). There is also evidence for a direct interaction between nervous, endocrine, and immune systems.…”

“…There is also evidence for a direct interaction between nervous, endocrine, and immune systems. Numerous mediators participating in this network and increased during sepsis behave as immunosuppressors: cortisol, norepinephrine, acetylcholine (66)(67)(68)(69)(70). However, they all need to be assessed in large clinical studies.…”