A novel lipid a from halomonas magadiensis inhibits enteric lPS-induced human monocyte activation

P. Maffia, A. Ialenti, P. Di Meglio, G. Grassia, M. Di Rosa, R. Lanzetta, A. Molinaro, A. Silipo, W. Grant, A. Ianaro

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29 Citations (Scopus)


Lipopolysaccharide (LPS) endotoxin is the bacterial product responsible for the clinical syndrome of Gram-negative septicemia and endotoxic shock. During sepsis, microbial antigens, such as LPS, activate monocytes and macrophages to produce several pro-inflammatory cytokines, among which tumor necrosis factor- (TNF-) appears to be very important for the development of endotoxic shock. The endotoxic properties of LPS principally reside in the lipid A (LIP A) component, which is the primary immunostimulatory center of Gram-negative bacteria. In recent years there has been a continuous effort to identify molecules able to antagonize the deleterious effects of endotoxic shock. In this study we show that a novel LIP A fraction from the LPS of Halomonas magadiensis (Hm), a Gram-negative extremophilic and alkaliphilic bacterium, significantly inhibits the synthesis of TNF- by human monocytes activated by Escherichia coli LPS. LIP A from Hm exerts these effects by interfering with E. coli LPS for activation of Toll-like receptor 4 expressed in human cells. This result defines Hm LIP A as a novel class of LPS antagonist whose structural features could be utilized for the design of compounds for the treatment of Gram-negative sepsis.

Original languageEnglish
Pages (from-to)354-360
Number of pages7
JournalEuropean Journal of Immunology
Publication statusPublished - 2006


  • halomonas magadiensis
  • toll-like receptor 4
  • Lipid A
  • monocytes


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