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10.1042/CS20150592

http://scihub22266oqcxt.onion/10.1042/CS20150592
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C4744094!4744094!26669797
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suck abstract from ncbi


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pmid26669797      Clin+Sci+(Lond) 2016 ; 130 (6): 451-61
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  • ENDOTHELIAL CELL TOLERANCE TO LIPOPOLYSACCHARIDE CHALLENGE IS INDUCED BY MONOPHOSPHORYL LIPID A #MMPMID26669797
  • Stark RJ; Choi H; Koch SR; Fensterheim BA; Lamb FS; Sherwood ER
  • Clin Sci (Lond) 2016[Mar]; 130 (6): 451-61 PMID26669797show ga
  • Prior exposure to lipopolysaccharide (LPS) produces a reduced or ?tolerant? inflammatory response to subsequent challenges with LPS, however the potent pro-inflammatory effects of LPS limit its clinical benefit. The adjuvant Monophosphoryl lipid A (MPLA) is a weak toll-like receptor 4 (TLR4) agonist that induces negligible inflammation but retains potent immunomodulatory properties. We postulated that pre-treatment with MPLA would inhibit the inflammatory response of endothelial cells to secondary LPS challenge. Human umbilical vein endothelial cells (HUVECs), were exposed to MPLA (10 µg/ml), LPS (100 ng/ml) or vehicle control. HUVECs were then washed and maintained in culture for 24 hours before being challenged with LPS (100 ng/ml). Supernatants were collected and examined for cytokine production in the presence or absence of siRNA inhibitors of critical TLR4 signaling proteins. Pretreatment with MPLA attenuated IL-6 production to secondary LPS challenge to a similar degree as LPS. The application of MyD88 siRNA dramatically reduced MPLA-induced tolerance while TRIF siRNA had no effect. The tolerant phenotype in endothelial cells was associated with reduced IKK, p38 and JNK phosphorylation and enhanced IRAK-M expression for LPS primed HUVECs, but less so in MPLA primed cells. Instead, MPLA-primed HUVECs demonstrated enhanced ERK phosphorylation. In contrast to leukocytes in which tolerance is largely TRIF-dependent, MyD88 signaling mediated endotoxin tolerance in endothelial cells. Most importantly, MPLA, a vaccine adjuvant with a wide therapeutic window, induced tolerance to LPS in endothelial cells.
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