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Substance P augments nitric oxide production and gene expression in murine macrophages

H K Jeon1, N P Jung, I H Choi

  • 1Department of Biology, Yonsei University, Seoul, South Korea. hkjeon@biology.yonsei.ac.kr

Immunopharmacology
|July 31, 1999
PubMed

Insights

Substance P (SP) boosts nitric oxide (NO) production in macrophages by increasing inducible NO synthase (iNOS) expression. This effect is blocked by NK-1 receptor antagonists and is more pronounced in stressed conditions, suggesting SP modulates macrophage NO production.

Area of Science:

  • Immunology
  • Neuroscience
  • Cell Biology

Background:

  • Nitric oxide (NO) is a crucial signaling molecule involved in immune responses.
  • Macrophages play a key role in innate and adaptive immunity.
  • Substance P (SP) is a neuropeptide with known immunomodulatory functions.

Purpose of the Study:

  • To investigate the effect of Substance P (SP) on nitric oxide (NO) synthase activity in macrophages.
  • To determine the role of SP in regulating inducible NO synthase (iNOS) expression.
  • To examine SP's influence on NO production in macrophages under stress conditions.

Main Methods:

  • Macrophages were stimulated with lipopolysaccharide (LPS) and SP.
  • Nitrite production was measured as an indicator of NO synthesis.
  • Expression of iNOS mRNA and protein was quantified.
  • An NK-1 receptor antagonist was used to assess receptor specificity.

Main Results:

  • SP significantly stimulated NO production in LPS-activated macrophages in a dose- and time-dependent manner.
  • The SP-induced NO production was inhibited by a specific NK-1 receptor antagonist.
  • SP increased both iNOS mRNA and protein levels in macrophages.
  • SP enhanced LPS-induced NO production in macrophages from cold-stressed mice.

Conclusions:

  • Substance P augments lipopolysaccharide-induced NO production in macrophages by enhancing iNOS expression.
  • The NK-1 receptor mediates the effects of SP on macrophage NO production.
  • SP plays a modulatory role in NO production by macrophages, particularly under stress.

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