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Volume 17, Number 6,
Issue of March 15, 1997
pp. 2181-2186
Copyright ©1997 Society for Neuroscience
 -MSH Modulates Local and Circulating Tumor Necrosis Factor-
in Experimental Brain Inflammation
Received Oct. 7, 1996; revised Dec. 23, 1996; accepted Dec. 31, 1996.
Nilum Rajora1,
Giovanni Boccoli4,
Dennis Burns3,
Sarita Sharma1,
Anna P. Catania4, and
James M. Lipton1, 2
Departments of 1 Physiology,
2 Anesthesiology and Pain Management, and
3 Pathology, University of Texas Southwestern Medical
Center at Dallas, Dallas, Texas 75235-9040, and 4 Clinica
Medica I, Ospedale Maggiore, Milan 20122, Italy
Tumor necrosis factor (TNF- ) underlies pathological processes
and functional disturbances in acute and chronic neurological disease and injury. The neuroimmunomodulatory peptide -MSH modulates actions and production of proinflammatory cytokines including TNF-,
but there is no prior evidence that it alters TNF- induced within
the brain. To test for this potential influence of the peptide, TNF-
was induced centrally by local injection of bacterial lipopolysaccharide (LPS). -MSH given once i.c.v. with LPS challenge, twice daily intraperitoneally (i.p.) for 5 d between central LPS injections, or both i.p. and centrally, inhibited production of TNF-
within brain tissue. Inhibition of TNF- protein formation by -MSH
was confirmed by inhibition of TNF- mRNA. Plasma TNF- concentration was elevated markedly after central LPS, indicative of an
augmented peripheral host response induced by the CNS signal. The
increase was inhibited by -MSH treatments, in relation to inhibition
of central TNF-. Presence within normal mouse brain of mRNA for the
-MSH receptor MC-1 suggests that the inhibitory effects of -MSH
on brain and plasma TNF- might be mediated by this receptor subtype.
The inhibitory effect of -MSH on brain TNF- did not depend on
circulating factors because the effect also occurred in brain tissue
in vitro. This indicates that -MSH can act directly
on brain cells to inhibit their production of TNF-. If central
TNF- contributes to pathology in CNS disease and injury, and
promotes inflammation in the periphery, agents that act on brain
-MSH receptors should decrease the pathological TNF- reaction and
promote tissue survival.
Key words:
-MSH;
TNF-;
modulation of CNS inflammation;
neurodegenerative disease;
LPS;
neuroimmunomodulation;
anti-inflammatory;
anticytokine
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