Antimicrobial peptide P18 inhibits inflammatory responses by LPS- but not by IFN-γ-stimulated macrophages

Yong Hai Nan, Young Jin Jeon, Il Seon Park, Song Yub Shin

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


Antimicrobial peptide P18 markedly inhibited the expression of inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α) and interleukin-1 beta (IL-1β) in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophage cells, whereas magainin 2 did not inhibit these activities. P18 dose-dependently reduced nitric oxide (NO) production by LPS-stimulated RAW 264.7 macrophage cells, with complete inhibition at 20 μg P18 ml -1. In contrast, P18 had no effect on NO production and the expression of iNOS mRNA and iNOS protein by interferon-gamma (IFN-γ)-stimulated RAW264.7 cells, suggesting P18 selectively inhibits LPS-stimulated inflammatory responses in macrophages. An LAL assay showed that P18 has strong LPS-neutralizing activity, indicating that P18 inhibits the inflammatory responses in LPS-stimulated macrophages by direct binding to LPS. Collectively, our results indicate that P18 has promising therapeutic potential as a novel anti-inflammatory as well as antimicrobial agent.

Original languageEnglish (US)
Pages (from-to)1183-1187
Number of pages5
JournalBiotechnology Letters
Issue number7
StatePublished - Jul 1 2008


  • Antimicrobial peptide
  • Inducible nitric oxide synthase
  • Interferon-gamma
  • Lipopolysaccharide
  • Nitric oxide
  • P18
  • Tumor necrosis factor-α


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