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Cathelicidin-Related Antimicrobial Peptide Negatively Regulates Bacterial Endotoxin-Induced Glial Activation

Anup Bhusal1,2, Youngpyo Nam1, Donggun Seo1

  • 1Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea.

Cells
|December 11, 2022
PubMed

Insights

Mouse cathelicidin-related antimicrobial peptide (CRAMP) limits neuroinflammation. CRAMP peptide treatment inhibited inflammatory responses in glial cells and the mouse brain, suggesting therapeutic potential.

Area of Science:

  • Neuroscience
  • Immunology
  • Microbiology

Background:

  • Mouse cathelicidin-related antimicrobial peptide (CRAMP) and human leucine-leucine-37 (LL-37) are key in innate immunity.
  • Bacterial endotoxin lipopolysaccharide (LPS) triggers neuroinflammation.

Purpose of the Study:

  • Investigate CRAMP's role in LPS-induced neuroinflammation.
  • Evaluate CRAMP peptide's therapeutic potential for neuroinflammatory conditions.

Main Methods:

  • In vitro studies of CRAMP on LPS-stimulated glial cells.
  • In vivo studies using an LPS-induced neuroinflammation mouse model.
  • Assessed CRAMP expression in astrocytes, microglia, and neurons.
  • Administered exogenous CRAMP via intraperitoneal and intracerebroventricular routes.

Main Results:

  • CRAMP peptide inhibited LPS-induced inflammatory activation of glial cells in culture.
  • CRAMP expression was upregulated in astrocytes, microglia, and neurons in LPS-treated mice.
  • Exogenous CRAMP significantly reduced inflammatory cytokine expression and glial cell reactivity in the mouse brain.
  • CRAMP demonstrated efficacy following both systemic and central LPS administration.

Conclusions:

  • CRAMP plays a crucial role in mitigating LPS-induced neuroinflammation.
  • CRAMP peptide shows promise as a therapeutic agent for bacterial infection-related neuroinflammatory disorders.
Keywords:
CRAMPLPSastrocytemicroglianeuroinflammation

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