Cathelicidin-Related Antimicrobial Peptide Negatively Regulates Bacterial Endotoxin-Induced Glial Activation.
Anup BhusalYoungpyo NamDonggun SeoWon-Ha LeeKyoungho SukPublished in: Cells (2022)
Recent studies have suggested that mouse cathelicidin-related antimicrobial peptide (CRAMP) and its human homologue leucine leucine-37 (LL-37) play critical roles in innate immune responses. Here, we studied the role of mouse CRAMP in bacterial endotoxin lipopolysaccharide (LPS)-induced neuroinflammation. CRAMP peptide treatment significantly inhibited LPS-mediated inflammatory activation of glial cells in culture. In the animal model of LPS-induced neuroinflammation, CRAMP expression was highly induced in multiple cell types, such as astrocytes, microglia, and neurons. Injection of exogenous CRAMP peptide significantly inhibited inflammatory cytokine expression and the reactivity of glial cells in the mouse brain following intraperitoneal or intracerebroventricular LPS administration. Altogether, results of the study suggest that CRAMP plays an important part in containment of LPS-induced neuroinflammatory responses, and that CRAMP can be exploited for the development of targeted therapies for neuroinflammatory conditions associated with bacterial infection.
Keyphrases
- lps induced
- inflammatory response
- immune response
- lipopolysaccharide induced
- induced apoptosis
- toll like receptor
- poor prognosis
- high glucose
- neuropathic pain
- oxidative stress
- endothelial cells
- cell cycle arrest
- diabetic rats
- drug induced
- spinal cord
- endoplasmic reticulum stress
- binding protein
- cell therapy
- signaling pathway
- long non coding rna
- brain injury
- induced pluripotent stem cells
- subarachnoid hemorrhage
- blood brain barrier