Neuropeptide α-MSH antagonizes IL-6- and TNF-induced fever
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The Melanocyte and the Epidermal Melanin Unit: An Expanded Concept
2007, Dermatologic ClinicsEndogenous antipyretics
2006, Clinica Chimica ActaCitation Excerpt :The evidence for a role of α-MSH as endogenous antipyretic was derived from the following sets of observations. Peripheral or central administration of α-MSH inhibits fever caused by LPS from Gram-negative bacteria, cell walls from Gram-positive bacteria, preparations of “endogenous pyrogen”, or individual cytokines [50–55]. Intracerebroventricular (i.c.v.) injection of an α-MSH antiserum [56] or chemical depletion of the central α-MSH sources in the arcuate nucleus [57] prolong or enhance fever.
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2002, Journal of Investigative DermatologyCitation Excerpt :The number of different tissues where α-MSH is released and where MC-R are expressed has led investigators to suggest roles other than cutaneous pigmentation and it is widely reported that α-MSH can inhibit fever, inflammation, and secretion of C reactive protein (Hiltz and Lipton, 1989;Hiltz et al, 1991;Lipton et al, 1991;1998;Martin et al, 1991;Catania and Lipton, 1993;Watanabe et al, 1993;Ceriani et al, 1994;Bhardwaj et al, 1996;Lipton and Catania, 1997;Orel et al, 1997;Rajora et al, 1997;Kalden et al, 1998a;1998b;Böhm et al, 1999;Ichiyama et al, 1999b;Taherzadeh et al, 1999). Inflammatory inhibition is thought to arise by an α-MSH signaling pathway that results in inhibiting the production or action of a number of proinflammatory cytokines [e.g., TNFα (Morandini et al, 1998), IL-1β (Weiss et al, 1991), or IL-6 (Martin et al, 1991)]. Evidence also exists on α-MSH directly stimulating the production of the IL-10 anti-inflammatory cytokine (Bhardwaj et al, 1996).