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10.1097/CCM.0000000000001566 http://scihub22266oqcxt.onion/10.1097/CCM.0000000000001566 C4833616!4833616!26757165     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26757165&cmd=llinks): Failed to open stream: HTTP request failed! 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Complement factor B production in renal tubular cells and its role in sodium transporter expression during polymicrobial sepsis |pdf=|usr=}}{{26757165}} gab.com Text Complement factor B production in renal tubular cells and its role in sodium transporter expression during polymicrobial sepsis JO: Crit Care Med http://www.kidney.de/pget.php?&tw=1&pmid=26757165 #FOAvip Objectives: Toll-like receptors (TLRs) and complement are two components of the innate immunity. Factor B (cfB) is essential for the alternative pathway (AP) of complement activation. We have recently reported that cfB is significantly up-regulated in the kidney and may contribute to acute tubular injury in an animal model of sepsis. The current study investigates the mechanisms responsible for the cfB up-regulation and its role in sodium transporter expression in tubular cells during sepsis. Design: Animal study. Setting: Laboratory investigation. Subjects: C57BL/6 J wide-type (WT), cfB?/?, and Nfkb1tm1Bal p50?/? mice. Interventions: Human proximal tubular cells (HK-2) and mouse tubular epithelial cells (MTECs) were stimulated with TLR agonists. Bay 11-7082 was used to block NF-?B pathway. AP activation was detected by C3 zymosan deposition. Polymicrobial sepsis was created by cecal ligation and puncture (CLP). Sodium transporter gene expression was determined by qRT-PCR. Measurements and Main Results: The agonists for TLR4 (LPS) or TLR3 (poly I:C) induced a marked increase in cfB expression in HK-2 and MTECs both at gene and protein levels. The TLR1/2 agonist, Pam3cys, induced cfB production only in HK-2 cells, not MTEC. The TLR9 ligand, CpG, failed to induce cfB production either in HK-2 cells or MTEC. LPS/poly I:C-induced cfB up-regulation was blocked by Bay 11-7082, a potent inhibitor of NF-?B signaling, and in MTECs deficient in p50 subunit of NF-?B. Media from the LPS-treated MTEC cultures contained de novo synthesized cfB and led to functional AP activation. In a CLP model, WT septic mice had down-regulated expression of sodium transporters in the kidney compared with the sham. In comparison, cfB?/? mice or mice treated with anti-cfB displayed preserved levels of Na+/K+ ATPase-?1 following sepsis. Conclusions: 1) TLR3/4 activation is sufficient to induce cfB production via NF-?B pathway and to enhance AP activation in the kidney tubular epithelial cells; 2) cfB may contribute to the down-regulation of certain sodium transporter expression during sepsis. Twit Text FOAVip Complement factor B production in renal tubular cells and its role in sodium transporter expression during polymicrobial sepsis ????Crit Care Med http://www.kidney.de/pget.php?&tw=1&pmid=26757165 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26757165 #FOAvip English Wikipedia <ref>{{Cite pmid|26757165}}</ref> Complement factor B production in renal tubular cells and its role in sodium transporter expression during polymicrobial sepsis #MMPMID26757165 Li D; Zou L; Feng Y; Xu G; Gong Y; Zhao G; Ouyang W; Thurman JM; Chao W Crit Care Med 2016[May]; 44 (5): e289-99 PMID26757165show ga Objectives: Toll-like receptors (TLRs) and complement are two components of the innate immunity. Factor B (cfB) is essential for the alternative pathway (AP) of complement activation. We have recently reported that cfB is significantly up-regulated in the kidney and may contribute to acute tubular injury in an animal model of sepsis. The current study investigates the mechanisms responsible for the cfB up-regulation and its role in sodium transporter expression in tubular cells during sepsis. Design: Animal study. Setting: Laboratory investigation. Subjects: C57BL/6 J wide-type (WT), cfB?/?, and Nfkb1tm1Bal p50?/? mice. Interventions: Human proximal tubular cells (HK-2) and mouse tubular epithelial cells (MTECs) were stimulated with TLR agonists. Bay 11-7082 was used to block NF-?B pathway. AP activation was detected by C3 zymosan deposition. Polymicrobial sepsis was created by cecal ligation and puncture (CLP). Sodium transporter gene expression was determined by qRT-PCR. Measurements and Main Results: The agonists for TLR4 (LPS) or TLR3 (poly I:C) induced a marked increase in cfB expression in HK-2 and MTECs both at gene and protein levels. The TLR1/2 agonist, Pam3cys, induced cfB production only in HK-2 cells, not MTEC. The TLR9 ligand, CpG, failed to induce cfB production either in HK-2 cells or MTEC. LPS/poly I:C-induced cfB up-regulation was blocked by Bay 11-7082, a potent inhibitor of NF-?B signaling, and in MTECs deficient in p50 subunit of NF-?B. Media from the LPS-treated MTEC cultures contained de novo synthesized cfB and led to functional AP activation. In a CLP model, WT septic mice had down-regulated expression of sodium transporters in the kidney compared with the sham. In comparison, cfB?/? mice or mice treated with anti-cfB displayed preserved levels of Na+/K+ ATPase-?1 following sepsis. Conclusions: 1) TLR3/4 activation is sufficient to induce cfB production via NF-?B pathway and to enhance AP activation in the kidney tubular epithelial cells; 2) cfB may contribute to the down-regulation of certain sodium transporter expression during sepsis. äComplement factor B production in renal tubular cells and its role in (epmc).pdf DeepDyve Pubget Overpricing