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Updated: May 21, 2026

Caenorhabditis elegans as a Model System for Discovering Bioactive Compounds Against Polyglutamine-Mediated Neurotoxicity

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Ingested (oral) neuropeptide Y inhibits EAE.

Staley A Brod¹, Victoria L Bauer

¹Department of Neurology, University of Texas — Houston, Health Science Center, Houston, TX 77030, United States. staley.a.brod@uth.tmc.edu

Journal of Neuroimmunology

|June 19, 2012

Summary

Oral neuropeptide Y (NPY) administration effectively reduced inflammation and clinical symptoms in experimental autoimmune encephalomyelitis (EAE). This study demonstrates NPY

Area of Science:

Neuroimmunology
Autoimmune Diseases
Inflammation Research

Background:

Previous studies show orally administered immunoactive proteins can modulate EAE.
These proteins include type I IFN, SIRS peptide 1-21, α-MSH, ACTH, and SST.
They inhibit EAE by altering cytokine profiles and regulatory T cell frequencies.

Purpose of the Study:

To investigate the anti-inflammatory potential of neuropeptide Y (NPY) in EAE.
To determine if oral NPY administration yields similar effects to other immunoactive proteins.

Main Methods:

Mice with MOG peptide-induced EAE were gavaged with NPY or saline.
Splenocytes from NPY-treated mice were adoptively transferred to recipient mice.
Cytokine profiles (Th1, Th2, Th17, IL-13) and clinical scores were analyzed.

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Main Results:

Oral NPY significantly inhibited ongoing EAE disease and reduced inflammation.
Adoptive transfer of NPY-fed donor cells conferred protection against EAE.
NPY modulated cytokine profiles, decreasing Th1/Th17 and increasing Th2-like IL-13 in the spleen and CNS.

Conclusions:

Orally administered NPY effectively inhibits clinical EAE and central nervous system (CNS) inflammation.
NPY achieves this by downregulating Th1/Th17 responses and upregulating Th2-like cytokines in the CNS.
NPY demonstrates therapeutic potential for autoimmune inflammatory conditions like EAE.