Anti-inflammatory properties of a novel peptide interleukin 1 receptor antagonist.
J Neuroinflammation
; 11: 27, 2014 Feb 03.
Article
en En
| MEDLINE
| ID: mdl-24490798
ABSTRACT
BACKGROUND:
Interleukin 1 (IL-1) is implicated in neuroinflammation, an essential component of neurodegeneration. We evaluated the potential anti-inflammatory effect of a novel peptide antagonist of IL-1 signaling, Ilantide.METHODS:
We investigated the binding of Ilantide to IL-1 receptor type I (IL-1RI) using surface plasmon resonance, the inhibition of Il-1ß-induced activation of nuclear factor κB (NF-κB) in HEK-Blue cells that contained an IL-1ß-sensitive reporter, the secretion of TNF-α in macrophages, protection against IL-1-induced apoptosis in neonatal pancreatic islets, and the penetration of Ilantide through the blood-brain barrier using competitive enzyme-linked immunosorbent assay (ELISA). We studied the effects of the peptide on social behavior and memory in rat models of lipopolysaccharide (LPS)- and amyloid-induced neuroinflammation, respectively, and its effect in a rat model of experimental autoimmune enchephalomyelitis.RESULTS:
Ilantide bound IL-1RI, inhibited the IL-1ß-induced activation of NF-κB, and inhibited the secretion of TNF-α in vitro. Ilantide protected pancreatic islets from apoptosis in vitro and reduced inflammation in an animal model of arthritis. The peptide penetrated the blood-brain barrier. It reduced the deficits in social activity and memory in LPS- and amyloid-treated animals and delayed the development of experimental autoimmune enchephalomyelitis.CONCLUSIONS:
These findings indicate that Ilantide is a novel and potent IL-1RI antagonist that is able to reduce inflammatory damage in the central nervous system and pancreatic islets.
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Oligopéptidos
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Artritis
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Encefalomielitis Autoinmune Experimental
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Proteína Antagonista del Receptor de Interleucina 1
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Antiinflamatorios
Tipo de estudio:
Prognostic_studies
Límite:
Animals
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Humans
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Male
Idioma:
En
Revista:
J Neuroinflammation
Asunto de la revista:
NEUROLOGIA
Año:
2014
Tipo del documento:
Article