2014 ; Vol.24-8: 1051~1058
|Author||Hangeun Kim, Bong Jun Jung, Jihye Jeong, Honam Chun, Dae Kyun Chung|
|Place of duty||School of Biotechnology and Institute of Life Science and Resources, Kyung Hee University, Yongin 449-701, Republic of Korea,RNA Inc., College of Life Science, Kyung Hee University, Yongin 449-701, Republic of Korea|
|Title||Lipoteichoic Acid from Lactobacillus plantarum Inhibits the Expression of Platelet-Activating Factor Receptor Induced by Staphylococcus aureus Lipoteichoic Acid or Escherichia coli Lipopolysaccharide in Human Monocyte-Like Cells|
J. Microbiol. Biotechnol.2014 ;
|Abstract||Platelet-activating factor receptor (PAFR) plays an important role in bacterial infection and
inflammation. We examined the effect of the bacterial cell wall components lipopolysaccharide
(LPS) and lipoteichoic acid (LTA) from Lactobacillus plantarum (pLTA) and Staphylococcus
aureus (aLTA) on PAFR expression in THP-1, a monocyte-like cell line. LPS and aLTA, but not
pLTA, significantly increased PAFR expression, whereas priming with pLTA inhibited LPSmediated
or aLTA-mediated PAFR expression. Expression of Toll-like receptor (TLR) 2 and 4,
and CD14 increased with LPS and aLTA treatments, but was inhibited by pLTA pretreatment.
Neutralizing antibodies against TLR2, TLR4, and CD14 showed that these receptors were
important in LPS-mediated or aLTA-mediated PAFR expression. PAFR expression is mainly
regulated by the nuclear factor kappa B signaling pathway. Blocking PAF binding to PAFR
using a PAFR inhibitor indicated that LPS-mediated or aLTA-mediated PAF expression
affected TNF-α production. In the mouse small intestine, pLTA inhibited PAFR, TLR2, and
TLR4 expression that was induced by heat-labile toxin. Our data suggested that pLTA has an
anti-inflammatory effect by inhibiting the expression of PAFR that was induced by pathogenic
|Key_word||Lactobacillus plantarum, Staphylococcus aureus, lipoteichoic acid, Platelet-activating factor, Toll-like receptor, Monocyte-like cells|
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