Inhibitory effects of Lactobacillus plantarum lipoteichoic acid (LTA) on Staphylococcus aureus LTA-induced tumor necrosis factor-alpha production.
Staphylococcus aureus is a common etiologic agent for Gram-positive sepsis, and its lipoteichoic acid (LTA) may be important in causing Gram-positive bacterial septic shock. Here, we demonstrate that highly purified LTA (pLTA) isolated from Lactobacillus plantarum inhibited aureus LTA (aLTA)-induced TNF-alpha production in THP- cells. Whereas pLTA scarcely induced TNF-alpha production, aLTA induced excessive TNF-alpha production. Interestingly, aLTA-induced TNF-alpha production was inhibited by pLTA pretreatment. Compared with pLTA, aLTA induced strong signal transduction through the MyD88, NF-kappaB, and MAP kinases. This signaling, however, was reduced by a pLTA pretreatment, and resulted in the inhibition of aLTA-induced TNF-alpha production. Whereas dealanylated LTAs, as well as native LTAs, contributed to TNF- induction or TNF-alpha reduction, deacylated LTAs did not, indicating that the acyl chain of LTA played an important role in the LTA-mediated immune regulation. These results suggest that pLTA may act as an antagonist for aLTA, and that an antagonistic pLTA may be a useful agent for suppressing the septic shock caused by Gram-positive bacteria.
Kim
Han Geun
HG
Graduate School of Biotechnology and Institute of Life Science and Resources, Kyung Hee University, Yongin, Korea.
Lee
Seung Yeon
SY
Kim
Na-Ra
NR
Ko
Mi Yeon
MY
Lee
Jung Min
JM
Yi
Tae-Hoo
TH
Chung
Sung Kyun
SK
Chung
Dae Kyun
DK
D045744:Cell Line, Tumor; D006801:Humans; D048191:Lactiplantibacillus plantarum / Q000737:chemistry* / Q000276:immunology; D018950:Lipopolysaccharide Receptors / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology / Q000494:pharmacology*; D016328:NF-kappa B / Q000276:immunology; D015398:Signal Transduction / Q000187:drug effects*; D013211:Staphylococcus aureus / Q000737:chemistry* / Q000276:immunology; D013682:Teichoic Acids / Q000276:immunology / Q000494:pharmacology*; D051195:Toll-Like Receptor 2 / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000096:biosynthesis*
D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D016328:NF-kappa B; C495342:TLR2 protein, human; D013682:Teichoic Acids; D051195:Toll-Like Receptor 2; D014409:Tumor Necrosis Factor-alpha; C009900:lipoteichoic acid