The inhibitory effect of ghrelin on sepsis-induced inflammation is mediated by the MAPK phosphatase-1

Asha Jacob, Derry Rajan, Betsy Pathickal, Imran Balouch, Adam Hartman, Rongqian Wu, Mian Zhou, Ping Wang

Research output: Contribution to journalArticlepeer-review

28 Scopus citations


Hepatocellular dysfunction occurs early in sepsis and this appears to be caused by Kupffer cell-derived TNF-α production from the liver as a result of the increased release of the sympathetic neurotransmitter, norepinephrine, from the gut. Ghrelin, a novel stomach-derived peptide, is down-regulated in sepsis and administration of ghrelin into rodents decrease pro-inflammatory cytokines, attenuates hepatic and other organ injuries and improves survival. Ghrelin's beneficial effect in sepsis is mediated by the inhibition of the sympathetic nervous system (SNS), as evidenced by the reduced gut-derived norepineprine (NE) release in sepsis after ghrelin treatment. Recent data suggest that MKP-1, the MAPK phosphatase-1, is involved in the innate immune responses. To determine that the beneficial effect of ghrelin in sepsis is mediated by MKP-1, rats were subjected to sepsis by cecal ligation and puncture (CLP) alone, or treated with ghrelin, beginning at 5-h post-CLP and liver tissues were harvested and examined for MKP-1 mRNA and protein expression. CLP alone produced a significant decrease in MKP-1 gene expression in liver tissues at 20 h after CLP (P

Original languageEnglish (US)
Pages (from-to)159-164
Number of pages6
JournalInternational Journal of Molecular Medicine
Issue number1
StatePublished - 2010
Externally publishedYes


  • Ghrelin
  • Inflammation
  • MAPK phosphatase-1
  • Norepinephrine
  • Sepsis

ASJC Scopus subject areas

  • Genetics


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