Lipoproteins in inflammation and sepsis. I. Basic science

Murch, Oliver; Collin, Marika; Hinds, C. J.; Thiemermann, Christoph

doi:10.1007/s00134-006-0432-y

Cited by 153 publications

(141 citation statements)

References 74 publications

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“…At the end of the 1970s, LPS was shown to be able to interact with HDL to form HDL-LPS complexes (27,28). Later, more evidence emerged showing that lipoproteins, especially HDL, were able to bind bacterial cell wall components, including lipoteichoic acid (12,29,30). H that in gram-negative arris et al (31) reported that preincubation of endotoxin with HDL or other lipoproteins before injection could protect animals against LPS-induced mortality.…”

Section: Discussionmentioning

confidence: 99%

Effect of lipid-bound apoA-I cysteine mutants on lipopolysaccharide-induced endotoxemia in mice

Wang

Zhu

et al. 2008

Journal of Lipid Research

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HDL has been shown to be able to neutralize the toxicity of lipopolysaccharide (LPS). Our previous study ( J. Lipid Res. 2005. 46: 1303-1311 characterized the properties of secondary structure and in vitro functions of different cysteine mutants of apolipoprotein A-I. Here, we reconstituted recombinant HDLs (named rHDLwt, rHDL52, rHDL74, rHDL107, rHDL129, rHDL173, rHDL195, and rHDL228) by mixing wild type or those mutants with dipalmitoyl phosphatidylcholine and examined their in vivo effects on LPS-induced endotoxemia in mice. Our results showed that 24 h after injection, mice receiving rHDL74 or rHDL52 had a significant decrease of plasma tumor necrosis factor a (TNF-a) and interleukin-1b (IL-1b), compared with control mice receiving either saline or rHDLwt (P , 0.05). Administration of rHDL74 to mice injected with LPS also led to a decrease of plasma IL-6, protection of lung against acute injury, and attenuation of endotoxin-induced clinical symptoms in mice, compared with controls injected with LPS only. However, injection of rHDL228 significantly increased plasma concentration of TNF-a and exacerbated LPS-induced lung injury. In summary, compared with rHDLwt, rHDL74 and rHDL52 exhibit higher anti-inflammation capabilities, whereas rHDL228 shows hyper-proinflammation by exacerbating LPS-induced endotoxemia in mice.-Wang, Y., X. Zhu, G. Wu, L. Shen, and B. Chen. Effect of lipid-bound apoA-I cysteine mutants on lipopolysaccharide-induced endotoxemia in mice.

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Section: Discussionmentioning

confidence: 99%

Effect of lipid-bound apoA-I cysteine mutants on lipopolysaccharide-induced endotoxemia in mice

Wang

Zhu

et al. 2008

Journal of Lipid Research

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“…HDL, as well as other plasma lipoproteins (LDL, TG-rich lipoproteins), can bind and neutralize Gram-negative bacterial LPS as well as Gram-positive bacterial lipoteichoic acid (LTA) Murch et al 2007). ApoA-I knockout mice, which lack HDL, exhibit decreased LPS neutralization in the serum compared with serum from control mice (Guo et al 2013); overexpression of apoA-I moderately improves survival compared to controls, suggesting that HDL elevation may protect against septic death.…”

Section: Interaction Of Hdl With Lps and Gram-negative Bacteriamentioning

confidence: 99%

HDL in Infectious Diseases and Sepsis

Pirillo

Catapano

Norata

2014

High Density Lipoproteins

166

163

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“…LIPOPOLYSACCHARIDE (LPS), a major component of the bacterial wall cell membrane, is released in the bloodstream during infection after bacteria are lysed by white blood cells (8,44). LPS binds to the Toll-like receptor 4 receptor complex on endothelial cells and induces multiple signaling pathways that lead to the production and release of proinflammatory cytokines and endothelial barrier dysfunction (EBD) (19,45,54).…”

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confidence: 99%

Histone deacetylase inhibitors prevent pulmonary endothelial hyperpermeability and acute lung injury by regulating heat shock protein 90 function

Joshi

Barabutis

Birmpas

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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In this study we assessed the role of HDAC in mediating lipopolysaccharide (LPS)-induced transendothelial hyperpermeability and acute lung injury (ALI). We demonstrate that HDAC inhibition protects against LPS-mediated EBD. Inhibition of multiple HDAC by the general inhibitors panobinostat or trichostatin provided protection against LPS-induced transendothelial hyperpermeability, acetylated and suppressed Hsp90 chaperone function, and attenuated RhoA activity and signaling crucial to endothelial barrier function. Treatment with the HDAC3-selective inhibitor RGFP-966 or the HDAC6-selective inhibitor tubastatin A provided partial protection against LPS-mediated transendothelial hyperpermeability. Similarly, knock down of HDAC3 and HDAC6 by specific small-interfering RNAs provided significant protection against LPS-induced EBD. Furthermore, combined pharmacological inhibition of both HDAC3 and -6 attenuated the inflammation, capillary permeability, and structural abnormalities associated with LPS-induced ALI in mice. Together these data indicate that HDAC mediate increased transendothelial hyperpermeability caused by LPS and that inhibition of HDAC protects against LPS-mediated EBD and ALI by suppressing Hsp90-dependent RhoA activity and signaling.

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Lipoproteins in inflammation and sepsis. I. Basic science

Cited by 153 publications

References 74 publications

Effect of lipid-bound apoA-I cysteine mutants on lipopolysaccharide-induced endotoxemia in mice

Effect of lipid-bound apoA-I cysteine mutants on lipopolysaccharide-induced endotoxemia in mice

HDL in Infectious Diseases and Sepsis

Histone deacetylase inhibitors prevent pulmonary endothelial hyperpermeability and acute lung injury by regulating heat shock protein 90 function

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