Curcumin decreases toll-like receptor-2 gene expression and function in human monocytes and neutrophils

Shuto, Tsuyoshi; Ono, Tomomi; Ohira, Yuko; Shimasaki, Shogo; Mizunoe, Shota; Watanabe, Kenji; Suico, Mary Ann; Koga, Tomoaki; Satō, Takashi; Morino, Saori; Sato, Keizo; Kai, Hirofumi

doi:10.1016/j.bbrc.2010.06.126

Cited by 21 publications

(19 citation statements)

References 32 publications

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“…TLRs may act as novel therapeutic targets for treating T cell-mediated liver diseases. Supporting our data, curcumin has recently been shown to prevent TLR2, TLR4 and TLR9 expression by other studies in vivo and in vitro [21][22][23]37]. Given that TLR2 and TLR4 are clearly responsible for the severity of inflammation induced by nonmicrobial agents, it has been postulated that endogenous molecules directly activate these TLRs [8].…”

Section: Discussionsupporting

confidence: 82%

“…Curcumin behaves as a TLR4 antagonist in vitro and inhibits LPS-TLR4 signaling in HEK-TLR4 cells [20]. Furthermore, in vitro or in vivo studies also showed that curcumin could inhibit TLR2, TLR4 and TLR9 expression [21][22][23]. Therefore, we deduced that curcumin might be useful in the treatment of inflammatory liver disease via inhibition of TLR2, TLR4 and TLR9 expression.…”

Section: Introductionmentioning

confidence: 88%

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Curcumin attenuates Concanavalin A-induced liver injury in mice by inhibition of Toll-like receptor (TLR) 2, TLR4 and TLR9 expression

Tu¹,

Han²,

Yao³

et al. 2012

International Immunopharmacology

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Section: Discussionsupporting

confidence: 82%

Section: Introductionmentioning

confidence: 88%

Curcumin attenuates Concanavalin A-induced liver injury in mice by inhibition of Toll-like receptor (TLR) 2, TLR4 and TLR9 expression

Tu¹,

Han²,

Yao³

et al. 2012

International Immunopharmacology

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“…So far, in different cell types, mainly inhibition of NF-κB, MAP kinases and Toll-like receptors have been shown to play a role [31,38-41]. …”

Section: Discussionmentioning

confidence: 99%

Curcuma DMSO extracts and curcumin exhibit an anti-inflammatory and anti-catabolic effect on human intervertebral disc cells, possibly by influencing TLR2 expression and JNK activity

et al. 2012

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BackgroundAs proinflammatory cytokines seem to play a role in discogenic back pain, substances exhibiting anti-inflammatory effects on intervertebral disc cells may be used as minimal-invasive therapeutics for intradiscal/epidural injection. The purpose of this study was to investigate the anti-inflammatory and anti-catabolic potential of curcuma, which has been used in the Indian Ayurvedic medicine to treat multiple ailments for a long time.MethodsHuman disc cells were treated with IL-1β to induce an inflammatory/catabolic cascade. Different extracts of curcuma as well as curcumin (= a component selected based on results with curcuma extracts and HPLC/MS analysis) were tested for their ability to reduce mRNA expression of proinflammatory cytokines and matrix degrading enzymes after 6 hours (real-time RT-PCR), followed by analysis of typical inflammatory signaling mechanisms such as NF-κB (Western Blot, Transcription Factor Assay), MAP kinases (Western Blot) and Toll-like receptors (real-time RT-PCR). Quantitative data was statistically analyzed using a Mann Whitney U test with a significance level of p < 0.05 (two-tailed).ResultsResults indicate that the curcuma DMSO extract significantly reduced levels of IL-6, MMP1, MMP3 and MMP13. The DMSO-soluble component curcumin, whose occurrence within the DMSO extract was verified by HPLC/MS, reduced levels of IL-1β, IL-6, IL-8, MMP1, MMP3 and MMP13 and both caused an up-regulation of TNF-α. Pathway analysis indicated that curcumin did not show involvement of NF-κB, but down-regulated TLR2 expression and inhibited the MAP kinase JNK while activating p38 and ERK.ConclusionsBased on its anti-inflammatory and anti-catabolic effects, intradiscal injection of curcumin may be an attractive treatment alternative. However, whether the anti-inflammatory properties in vitro lead to analgesia in vivo will need to be confirmed in an appropriate animal model.

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“…Cell Culture, Isolation of Primary cells-Primary peripheral blood monocytes (MC) and polymorphonuclear neutrophils (PMN) were isolated from heparinized venous blood of healthy individuals by following the suggested protocols using FicollPaque PLUS (Amersham Biosciences) as indicated before (16). Briefly, the whole blood was mixed with 0.9% sodium chloride containing 3% dextran 500 (Sigma) and incubated at room temperature for 30 min to sediment erythrocytes.…”

Section: Methodsmentioning

confidence: 99%

Lipopolysaccharide Decreases Single Immunoglobulin Interleukin-1 Receptor-related Molecule (SIGIRR) Expression by Suppressing Specificity Protein 1 (Sp1) via the Toll-like Receptor 4 (TLR4)-p38 Pathway in Monocytes and Neutrophils

Ueno-Shuto

Kato

Tasaki

et al. 2014

Journal of Biological Chemistry

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Background: Single immunoglobulin interleukin-1 receptor-related molecule (SIGIRR) is a negative inflammatory regulator whose regulatory mechanism is mainly described in epithelial tissues. Results: Higher monocytic and neutrophilic SIGIRR expression is maintained by Sp1. Conclusion: Lipopolysaccharide decreases SIGIRR expression by suppressing Sp1 via the TLR4-p38 pathway. Significance: The LPS-dependent SIGIRR down-regulation may be critical for optimal inflammatory responses in immune cells.

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Curcumin decreases toll-like receptor-2 gene expression and function in human monocytes and neutrophils

Cited by 21 publications

References 32 publications

Curcumin attenuates Concanavalin A-induced liver injury in mice by inhibition of Toll-like receptor (TLR) 2, TLR4 and TLR9 expression

Curcumin attenuates Concanavalin A-induced liver injury in mice by inhibition of Toll-like receptor (TLR) 2, TLR4 and TLR9 expression

Curcuma DMSO extracts and curcumin exhibit an anti-inflammatory and anti-catabolic effect on human intervertebral disc cells, possibly by influencing TLR2 expression and JNK activity

Lipopolysaccharide Decreases Single Immunoglobulin Interleukin-1 Receptor-related Molecule (SIGIRR) Expression by Suppressing Specificity Protein 1 (Sp1) via the Toll-like Receptor 4 (TLR4)-p38 Pathway in Monocytes and Neutrophils

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