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10.1186/s12974-019-1538-9 http://scihub22266oqcxt.onion/10.1186/s12974-019-1538-9 C6637517!6637517!31319868     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Neuroinflammation 2019 ; 16 (ä): ä Nephropedia Template TP {{tp|p=31319868|t=2019. Ciprofloxacin and levofloxacin attenuate microglia inflammatory response via TLR4/NF-kB pathway |pdf=|usr=}}{{31319868}} gab.com Text Ciprofloxacin and levofloxacin attenuate microglia inflammatory response via TLR4/NF-kB pathway JO: J Neuroinflammation http://www.kidney.de/pget.php?&tw=1&pmid=31319868 #FOAvip Background: Neuroinflammation is the response of the central nervous system to events that interfere with tissue homeostasis and represents a common denominator in virtually all neurological diseases. Activation of microglia, the principal immune effector cells of the brain, contributes to neuronal injury by release of neurotoxic products. Toll-like receptor 4 (TLR4), expressed on the surface of microglia, plays an important role in mediating lipopolysaccharide (LPS)-induced microglia activation and inflammatory responses. We have previously shown that curcumin and some of its analogues harboring an ?,?-unsaturated 1,3-diketone moiety, able to coordinate the magnesium ion, can interfere with LPS-mediated TLR4?myeloid differentiation protein-2 (MD-2) signaling. Fluoroquinolone (FQ) antibiotics are compounds that contain a keto-carbonyl group that binds divalent ions, including magnesium. In addition to their antimicrobial activity, FQs are endowed with immunomodulatory properties, but the mechanism underlying their anti-inflammatory activity remains to be defined. The aim of the current study was to elucidate the molecular mechanism of these compounds in the TLR4/NF-?B inflammatory signaling pathway. Methods: The putative binding mode of five FQs [ciprofloxacin (CPFX), levofloxacin (LVFX), moxifloxacin, ofloxacin, and delafloxacin] to TLR4?MD-2 was determined using molecular docking simulations. The effect of CPFX and LVFX on LPS-induced release of IL-1? and TNF-? and NF-?B activation was investigated in primary microglia by ELISA and fluorescence staining. The interaction of CPFX and LVFX with TLR4?MD-2 complex was assessed by immunoprecipitation followed by Western blotting using Ba/F3 cells. Results: CPFX and LVFX bound to the hydrophobic region of the MD-2 pocket and inhibited LPS-induced secretion of pro-inflammatory cytokines and activation of NF-?B in primary microglia. Furthermore, these FQs diminished the binding of LPS to TLR4?MD-2 complex and decreased the resulting TLR4?MD-2 dimerization in Ba/F3 cells. Conclusions: These results provide new insight into the mechanism of the anti-inflammatory activity of CPFX and LVFX, which involves, at least in part, the activation of TLR4/NF-?B signaling pathway. Our findings might facilitate the development of new molecules directed at the TLR4?MD-2 complex, a potential key target for controlling neuroinflammation. Electronic supplementary material: The online version of this article (10.1186/s12974-019-1538-9) contains supplementary material, which is available to authorized users. Twit Text FOAVip Ciprofloxacin and levofloxacin attenuate microglia inflammatory response via TLR4/NF-kB pathway ????J Neuroinflammation http://www.kidney.de/pget.php?&tw=1&pmid=31319868 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31319868 #FOAvip English Wikipedia <ref>{{Cite pmid|31319868}}</ref> Ciprofloxacin and levofloxacin attenuate microglia inflammatory response via TLR4/NF-kB pathway #MMPMID31319868 Zusso M; Lunardi V; Franceschini D; Pagetta A; Lo R; Stifani S; Frigo AC; Giusti P; Moro S J Neuroinflammation 2019[]; 16 (ä): ä PMID31319868show ga Background: Neuroinflammation is the response of the central nervous system to events that interfere with tissue homeostasis and represents a common denominator in virtually all neurological diseases. Activation of microglia, the principal immune effector cells of the brain, contributes to neuronal injury by release of neurotoxic products. Toll-like receptor 4 (TLR4), expressed on the surface of microglia, plays an important role in mediating lipopolysaccharide (LPS)-induced microglia activation and inflammatory responses. We have previously shown that curcumin and some of its analogues harboring an ?,?-unsaturated 1,3-diketone moiety, able to coordinate the magnesium ion, can interfere with LPS-mediated TLR4?myeloid differentiation protein-2 (MD-2) signaling. Fluoroquinolone (FQ) antibiotics are compounds that contain a keto-carbonyl group that binds divalent ions, including magnesium. In addition to their antimicrobial activity, FQs are endowed with immunomodulatory properties, but the mechanism underlying their anti-inflammatory activity remains to be defined. The aim of the current study was to elucidate the molecular mechanism of these compounds in the TLR4/NF-?B inflammatory signaling pathway. Methods: The putative binding mode of five FQs [ciprofloxacin (CPFX), levofloxacin (LVFX), moxifloxacin, ofloxacin, and delafloxacin] to TLR4?MD-2 was determined using molecular docking simulations. The effect of CPFX and LVFX on LPS-induced release of IL-1? and TNF-? and NF-?B activation was investigated in primary microglia by ELISA and fluorescence staining. The interaction of CPFX and LVFX with TLR4?MD-2 complex was assessed by immunoprecipitation followed by Western blotting using Ba/F3 cells. Results: CPFX and LVFX bound to the hydrophobic region of the MD-2 pocket and inhibited LPS-induced secretion of pro-inflammatory cytokines and activation of NF-?B in primary microglia. Furthermore, these FQs diminished the binding of LPS to TLR4?MD-2 complex and decreased the resulting TLR4?MD-2 dimerization in Ba/F3 cells. Conclusions: These results provide new insight into the mechanism of the anti-inflammatory activity of CPFX and LVFX, which involves, at least in part, the activation of TLR4/NF-?B signaling pathway. Our findings might facilitate the development of new molecules directed at the TLR4?MD-2 complex, a potential key target for controlling neuroinflammation. Electronic supplementary material: The online version of this article (10.1186/s12974-019-1538-9) contains supplementary material, which is available to authorized users. äCiprofloxacin and levofloxacin attenuate microglia inflammatory respon(epmc).pdf DeepDyve Pubget Overpricing