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10.4049/jimmunol.1501709

http://scihub22266oqcxt.onion/10.4049/jimmunol.1501709
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C4856165!4856165!26936883
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suck abstract from ncbi


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pmid26936883      J+Immunol 2016 ; 196 (7): 3135-47
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  • Human SR-BI and SR-BII potentiate LPS-induced inflammation and acute liver and kidney injury in mice #MMPMID26936883
  • Baranova IN; Souza ACP; Bocharov AV; Vishnyakova TG; Hu X; Vaisman BL; Amar MJ; Chen Z; Kost Y; Remaley AT; Patterson AP; Yuen PST; Star RA; Eggerman TL
  • J Immunol 2016[Apr]; 196 (7): 3135-47 PMID26936883show ga
  • The class B scavenger receptors BI (SR-BI) and BII (SR-BII) are HDL receptors that recognize various pathogens, including bacteria and their products. It has been reported that SR-BI/II-null mice are more sensitive than normal mice to endotoxin-induced inflammation and sepsis. Since the SR-BI/II-knockout model demonstrates multiple immune and metabolic disorders we investigated the role of each receptor in the LPS-induced inflammatory response and tissue damage using transgenic mice with pLiv-11-directed expression of human SR-BI or SR-BII. Six hours after intraperitoneal LPS injection, transgenic hSR-BI and hSR-BII mice demonstrated markedly higher serum levels of pro-inflammatory cytokines and 2-3-fold increased expression levels of inflammatory mediators in the liver and kidney, compared to wild type (WT) mice. LPS-stimulated iNOS expression was 3-6-fold higher in the liver and kidney of both transgenic strains, although serum NO levels were similar in all mice. Despite the lower HDL plasma levels, both transgenic strains responded to LPS by a 5-fold increase of plasma corticosterone levels which were only moderately lower than in WT animals. LPS treatment resulted in MAPKs activation in tissues of all mice; however, the strongest response was detected for hepatic ERK1/2 and kidney JNK of both transgenic mice. Histological examination of hepatic and renal tissue from LPS-challenged mice revealed more injury in hSR-BII but not hSR-BI transgenic mice vs WT controls. Our findings demonstrate that hSR-BII, and to a lesser extent hSR-BI, significantly increase LPS-induced inflammation and contribute to LPS-induced tissue injury in the liver and kidney, two major organs susceptible to LPS toxicity.
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