Oxidized Phospholipid Inhibition of Toll-like Receptor (TLR) Signaling Is Restricted to TLR2 and TLR4

Erridge, Clett; Kennedy, Simon; Spickett, Corinne M.; Webb, David J.

doi:10.1074/jbc.m800352200

Cited by 213 publications

(132 citation statements)

References 55 publications

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“…Then, LPSs were assessed in bone marrow-derived macrophages (BMDMs) in the presence or absence of Oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (OxPAPC)C (40 μg/mL; Fig. S3D), which inhibits the signaling induced by the bacterial LPS (35).…”

Section: Activation Of Nf-κb By Lps Extracted From Acellular and Intrmentioning

confidence: 99%

IntracellularShigellaremodels its LPS to dampen the innate immune recognition and evade inflammasome activation

Paciello¹,

Silipo

Fazio³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Section: Activation Of Nf-κb By Lps Extracted From Acellular and Intrmentioning

confidence: 99%

IntracellularShigellaremodels its LPS to dampen the innate immune recognition and evade inflammasome activation

Paciello¹,

Silipo

Fazio³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…When LBP binds lipid A in LPS, a CD14-LPS complex forms. LBP is involved in phospholipid transfer, and disassociates LPS from its oligomeric state into monomers (29). Depolymerized LPS binds to TLR4, leading to polymerization and activation of TLR4.…”

Section: Discussionmentioning

confidence: 99%

Penehyclidine ameliorates acute lung injury by inhibiting Toll-like receptor 2/4 expression and nuclear factor-κB activation

Wang

Che

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. The aim of the present study was to investigate the effect of penehyclidine (PHC) on endotoxin-induced acute lung injury (ALI), as well as to examine the mechanism underlying this effect. A total of 60 rats were randomly divided into five groups, including the control (saline), LPS and three LPS + PHC groups. ALI was induced in the rats by injection of 8 mg lipopolysaccharide (LPS)/kg body weight. The rats were then treated with or without PHC at 0.3, 1 or 3 mg/kg body weight 1 min following LPS injection. After 6 h, serum levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6 were determined by ELISA. In addition, the mRNA expression levels of toll-like receptor (TLR)2 and TLR4 were examined by reverse transcription-quantitative polymerase chain reaction in the lung tissue samples, and nuclear factor (NF)-κB p65 protein expression levels were examined by western blot analysis. The results demonstrated that lung injury was ameliorated by treatment with PHC (1 and 3 mg/kg body weight) as compared with treatment with LPS alone. Injection of LPS significantly increased the mRNA expression levels of TLR2 and TLR4, as well as the protein expression levels of NF-κB p65 in the lung tissue samples. Serum levels of TNF-α and IL-6 were also upregulated by LPS injection. Treatment of the rats with PHC following LPS injection suppressed the LPS-induced increase in TLR2/4 mRNA and NF-κB p65 protein expression levels. PHC also inhibited the increase in TNF-α and IL-6 serum levels. In addition, PHC reduced LPS-induced ALI and decreased the serum levels of TNF-α and IL-6, possibly by downregulating TLR2/4 mRNA expression and inhibiting NF-κB activity, and consequently alleviating the inflammatory response.

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“…OxPLs also interact and bind with other recognition receptors in macrophages such as TLRs, CD14, LPS binding protein and C-reactive protein competing with negative ligands , Erridge et al 2008, Miller et al 2003. Thus, the formation of OxPLs during inflammation may represent an important feedback mechanism to limit further tissue damage.…”

Section: Regulation Of Vascular Cell Functionmentioning

confidence: 99%

“…OxPAPC also induces lung injury and IL-6 production by mouse lung macrophages via the TLR4-TRIF-TRAF6 pathway (Imai et al 2008). On the other hand various classes of OxPLs do not influence the basal levels of E-selectin, ICAM-1, VCAM-1, TNFa, IL-6, IL-1a, IL-1b, and COX-2 in whole blood or individual cell types, including human umbilical vein ECs, blood monocytes, macrophage cell line, or fibroblasts , Erridge et al 2008.…”

Section: Toll-like Receptormentioning

confidence: 99%

Oxidized Phospholipids: Introduction and Biological Significance

Ashraf¹,

Srivastava²

2012

Lipoproteins - Role in Health and Diseases

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Oxidized Phospholipid Inhibition of Toll-like Receptor (TLR) Signaling Is Restricted to TLR2 and TLR4

Cited by 213 publications

References 55 publications

IntracellularShigellaremodels its LPS to dampen the innate immune recognition and evade inflammasome activation

IntracellularShigellaremodels its LPS to dampen the innate immune recognition and evade inflammasome activation

Penehyclidine ameliorates acute lung injury by inhibiting Toll-like receptor 2/4 expression and nuclear factor-κB activation

Oxidized Phospholipids: Introduction and Biological Significance

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