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Adjuvant Activity of Mycobacterium paratuberculosis in Enhancing the Immunogenicity of Autoantigens During Experimental Autoimmune Encephalomyelitis
06:57

Adjuvant Activity of Mycobacterium paratuberculosis in Enhancing the Immunogenicity of Autoantigens During Experimental Autoimmune Encephalomyelitis

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Ingested (oral) ACTH inhibits EAE.

Staley A Brod1, Zachary M Hood

  • 1Department of Neurology, University of Texas-Houston, Health Science Center, 6431 Fannin St, Houston, TX 77030, United States. staley.a.brod@uth.tmc.edu

Journal of Neuroimmunology
|November 18, 2010
PubMed
Summary
This summary is machine-generated.

Oral administration of adrenocorticotropic hormone (ACTH) effectively reduced inflammation and disease severity in experimental autoimmune encephalomyelitis (EAE). This suggests ACTH

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Published on: September 9, 2022

Area of Science:

  • Neuroimmunology
  • Autoimmune Diseases
  • Endocrinology

Background:

  • Experimental autoimmune encephalomyelitis (EAE) is a model for multiple sclerosis.
  • Type I interferon and SIRS peptide have shown anti-inflammatory effects in EAE.
  • The immunoactive protein ACTH's potential anti-inflammatory role in EAE is unexplored.

Purpose of the Study:

  • To investigate the anti-inflammatory effects of orally administered ACTH in a mouse model of EAE.
  • To determine the impact of ACTH on immune cell populations and cytokine profiles in EAE.

Main Methods:

  • B6 mice were induced with EAE and gavaged with saline or ACTH at disease onset.
  • Clinical scores and inflammatory foci were assessed.
  • Cytokine levels (IL-17, IL-2, IFN-γ, IL-4, M-CSF) and immune cell populations (CD4+CD25+FoxP3+) were analyzed.
  • Adoptive transfer experiments were performed using splenocytes from ACTH-treated or control mice.

Main Results:

  • ACTH administration significantly decreased clinical scores and central nervous system (CNS) inflammatory foci.
  • ACTH treatment reduced T(eff) (IL-17) and Th1-like cytokines (IL-2, IFN-γ) while increasing immunoregulatory IL-4 and M-CSF.
  • Adoptive transfer of ACTH-fed splenocytes suppressed EAE severity, correlating with altered cytokine profiles and increased regulatory T cells (CD4+CD25+FoxP3+).

Conclusions:

  • Oral ACTH exhibits significant anti-inflammatory and disease-suppressing effects in EAE.
  • The protective mechanism involves modulation of T(eff) and Th1 cytokines, alongside enhanced immunoregulatory cytokines and regulatory T cell populations.
  • ACTH directly impacts the immune system, offering a potential therapeutic strategy for autoimmune neuroinflammation.