PMID- 8127402
OWN - NLM
STAT- MEDLINE
DCOM- 19940414
LR  - 20180214
IS  - 0028-3835 (Print)
IS  - 0028-3835 (Linking)
VI  - 59
IP  - 2
DP  - 1994 Feb
TI  - Central neurogenic antiinflammatory action of alpha-MSH: modulation of peripheral 
      inflammation induced by cytokines and other mediators of inflammation.
PG  - 138-43
AB  - The neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) has potent 
      antipyretic and antiinflammatory properties. When administered systemically, the 
      naturally occurring molecule and its COOH-terminal tripeptide sequence inhibit 
      inflammation induced by peripherally applied irritants and intradermal injections 
      of mediators of inflammation such as interleukin-1 (IL-1), interleukin-6 (IL-6), 
      and tumor necrosis factor-alpha (TNF alpha). We recently found that alpha-MSH can 
      act solely within the brain to inhibit inflammation caused by a general irritant 
      applied to the skin. This activity appears to be shared with salicylate drugs and 
      the combined observations suggest the existence of descending neurogenic 
      antiinflammatory signals capable of modulating inflammation in peripheral 
      tissues. To improve our knowledge of the scope of this action of the peptide, 
      alpha-MSH was injected into the cerebral ventricles (i.c.v.) of mice that had 
      received intradermal injections in the ear of mediators of inflammation: IL-1 
      beta, IL-8, leukotriene B4, and platelet-activating factor. The centrally 
      administered peptide inhibited the actions of all of these proinflammatory agents 
      as determined from comparisons with measures of ear edema over time in control 
      animals; this indicates that the central peptide can alter inflammation induced 
      in the periphery by major mediators of inflammation. In tests confined to IL-1 
      beta, central administration of alpha-MSH(11-13) was also effective. These 
      findings support the concept of a descending neurogenic antiinflammatory 
      influence promoted by an action of alpha-MSH within the brain, an inhibitory 
      influence that is not restricted to modulation of just one or a limited set of 
      the mediators of inflammation.
FAU - Ceriani, G
AU  - Ceriani G
AD  - Physiology Department, University of Texas Southwestern Medical Center at Dallas 
      75235-9040.
FAU - Macaluso, A
AU  - Macaluso A
FAU - Catania, A
AU  - Catania A
FAU - Lipton, J M
AU  - Lipton JM
LA  - eng
GR  - NS10046/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Switzerland
TA  - Neuroendocrinology
JT  - Neuroendocrinology
JID - 0035665
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-8)
RN  - 0 (Platelet Activating Factor)
RN  - 1HGW4DR56D (Leukotriene B4)
RN  - 581-05-5 (alpha-MSH)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents, Non-Steroidal/*therapeutic use
MH  - *Cytokines/administration & dosage
MH  - Edema/chemically induced/drug therapy
MH  - Female
MH  - Inflammation/chemically induced/*drug therapy
MH  - Injections, Intraventricular
MH  - Interleukin-1/administration & dosage
MH  - Interleukin-8/administration & dosage
MH  - Leukotriene B4/administration & dosage
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Platelet Activating Factor/administration & dosage
MH  - alpha-MSH/administration & dosage/*therapeutic use
EDAT- 1994/02/01 00:00
MHDA- 1994/02/01 00:01
CRDT- 1994/02/01 00:00
PHST- 1994/02/01 00:00 [pubmed]
PHST- 1994/02/01 00:01 [medline]
PHST- 1994/02/01 00:00 [entrez]
AID - 10.1159/000126650 [doi]
PST - ppublish
SO  - Neuroendocrinology. 1994 Feb;59(2):138-43. doi: 10.1159/000126650.