Signaling pathways involved in LPS induced TNFalpha production in human adipocytes

Hoareau, Laurence; Bencharif, Karima; Rondeau, Philippe; Murumalla, Ravi Kumar; Ravanan, Palaniyandi; Tallet, Frank; Delarue, Pierre; Césari, Maya; Roche, Régis; Festy, Franck

doi:10.1186/1476-9255-7-1

Cited by 84 publications

(76 citation statements)

References 40 publications

(38 reference statements)

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“…These inhibitors have no intrinsic effects on cell death and IL-6 secretion (data not shown) and were previously controlled for their efficiency. 7 A strong and significant inhibition of HMGB1-induced IL-6 secretion was shown when NF-kB and P38 MAPK inhibitors were co-incubating with HMGB1, which indicates the involvement of NF-kB and P38 MAPK in the disulfide HMGB1 signaling (Fig. 2).…”

Section: Resultsmentioning

confidence: 99%

TLR4-dependant pro-inflammatory effects of HMGB1 on human adipocyte

et al. 2016

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Chronic low grade inflammation is one of the major metabolic disorders in case of obesity and associated pathologies. By its important secretion function, the role of adipose tissue in this metabolic low grade inflammation is well known. Recently, it was demonstrated that the alarmin high mobility group box protein 1 (HMGB1) is involved in obesity-related pathologies by its increased serum levels in obese compared to normal weight individuals, and by its proinflammatory effects. However, the role of HMGB1 on adipocytes inflammation is poorly documented and we propose to investigate this point. Primary culture of human subcutaneous adipocytes were performed from human adipose tissue samples. Cells were treated with recombinant HMGB1 with/without anti-TLR4 antibody and inhibitors of NF-kB and P38 MAPK. Supernatants were collected for IL-6 and MCP-1 ELISA. HMGB1 initiates Toll-like receptor 4 (TLR4)-dependent activation of inflammation through the downstream NF-kB and P38 MAPK signaling pathway to upregulate the secretion of the pro-inflammatory cytokine IL-6. HMGB1 has proinflammatory effects on adipocytes. This reinforces the role of TLR4 in adipose tissue inflammation and antagonizing the HMGB1 inflammatory pathway could bring on new therapeutic targets to counteract obesity-associated pathologies.

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Section: Resultsmentioning

confidence: 99%

TLR4-dependant pro-inflammatory effects of HMGB1 on human adipocyte

et al. 2016

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“…We speculate that TNF-a production may not solely be dependent on the NF-jB mediated pathway; there may be other pathway(s) that can also regulate TNF-a production. Indeed, Hoareau et al 71 showed that both NF-jB and the p38 MAP Kinase pathway could be involved in TNF-a secretion.…”

Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Effects of Lutein in Retinal Ischemic/Hypoxic Injury: In Vivo and In Vitro Studies

Fung

et al. 2012

Invest. Ophthalmol. Vis. Sci.

114

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PURPOSE. Lutein protects retinal neurons by its anti-oxidative and anti-apoptotic properties in ischemia/reperfusion (I/R) injury while its anti-inflammatory effects remain unknown. As Müller cells play a critical role in retinal inflammation, the effect of lutein on Müller cells was investigated in a murine model of I/R injury and a culture model of hypoxic damage.METHODS. Unilateral retinal I/R was induced by a blockade of internal carotid artery using the intraluminal method in mice. Ischemia was maintained for 2 hours followed by 22 hours of reperfusion, during which either lutein (0.2 mg/kg) or vehicle was administered. Flash electroretinogram (flash ERG) and glial fibrillary acidic protein (GFAP) activation were assessed. Lutein's effect on Müller cells was further evaluated in immortalized rat Müller cells (rMC-1) challenged with cobalt chloride-induced hypoxia. Levels of IL-1b, cyclooxygenase-2 (Cox-2), TNFa, and nuclear factor-NF-kappa-B (NF-jB) were examined by Western blot analysis. RESULTS.Lutein treatment minimized deterioration of b-wave/awave ratio and oscillatory potentials as well as inhibited upregulation of GFAP in retinal I/R injury. In cultured Müller cells, lutein treatment increased cell viability and reduced level of nuclear NF-jB, IL-1b, and Cox-2, but not TNFa after hypoxic injury.CONCLUSIONS. Reduced gliosis in I/R retina was observed with lutein treatment, which may contribute to preserved retinal function. Less production of pro-inflammatory factors from Müller cells suggested an anti-inflammatory role of lutein in retinal ischemic/hypoxic injury. Together with our previous studies, our results suggest that lutein protected the retina from ischemic/hypoxic damage by its anti-oxidative, antiapoptotic, and anti-inflammatory properties. (Invest Ophthalmol Vis Sci. 2012;53:5976-5984)

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“…Multiple mammalian receptors for LPS have been identified such as b 2 -integrins CD11/CD18, the macrophage scavenger receptor for acetylated LDL, L-selectin and the most important CD14. LPS activates a number of intracellular signaling pathways, including IkB kinase-nuclear factor kB (NFkB) pathway and three mitogen-activated protein kinase pathways [16,17] . These pathways phosphorylate and activate various transcription factors, including NFkB/Rel proteins, activator protein 1 (AP-1) and nuclear factor-IL-6 (NF-IL6).…”

Section: Cell Signaling Networkmentioning

confidence: 99%