Heparin‐like polymers modulate proinflammatory cytokine production by lipopolysaccharide‐stimulated human monocytes

Anastase-Ravion, Sylvie; Carreno, Marie‐Paule; Blondin, Catherine; Ravion, Olivier; Champion, J.; Chaubet, Fréderic; Haeffner‐Cavaillon, Nicole; Letourneur, Didier

doi:10.1002/jbm.10112

Cited by 19 publications

(5 citation statements)

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“…Many fucans have the property of inhibiting the synthesis of cytokines, such as a fucan extracted from Ascophyllum nodosum , which has the ability to modulate the production of TNF-α and IL-6 when stimulated with lipopolysaccharides (LPS) [29]. Therefore, in order to understand the mechanism of leukocyte migration evoked by F2.0v, we evaluated the effect of this fucan in cytokine (TNF-α, interleukin 1β (IL-1β) and interleukin 6 (IL-6)) release.…”

Section: Resultsmentioning

confidence: 99%

Evaluation of Anti-Nociceptive and Anti-Inflammatory Activities of a Heterofucan from Dictyota menstrualis

et al. 2013

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Fucan is a term that defines a family of homo- and hetero-polysaccharides containing sulfated l-fucose in its structure. In this work, a heterofucan (F2.0v) from the seaweed, Dictyota menstrualis, was evaluated as an antinociceptive and anti-inflammatory agent. F2.0v (20.0 mg/kg) inhibits 100% of leukocyte migration into the peritoneal cavity after chemical stimulation. However, F2.0v does not alter the expression of interleukin-1 beta (IL-1β) and interleukin-6 (IL-6), as well as tumor necrosis factor alpha (TNF-α). F2.0v (20.0 mg/kg) has peripheral antinociceptive activity with potency similar to dipyrone. On the other hand, it had no effect on pain response on the hot plate test. Confocal microscopy analysis and flow cytometry showed that F2.0v binds to the surface of leucocytes, which leads us to suggest that the mechanism of action of anti-inflammatory and antinociceptive F2.0v is related to its ability to inhibit the migration of leukocytes to the site of tissue injury. In summary, the data show that F2.0v compound has great potential as an antinociceptive and anti-inflammatory, and future studies will be performed to further characterize the mechanism of action of F2.0v.

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Section: Resultsmentioning

confidence: 99%

Evaluation of Anti-Nociceptive and Anti-Inflammatory Activities of a Heterofucan from Dictyota menstrualis

et al. 2013

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“…It has been shown that heparin anti-inflammatory effect could be produced by the inhibition of NF-κ≡ nuclear translocation into the lung, 18 26 reducing the expression of TNF-α and IL-6. 25 28 31 This is consistent with our results.…”

Section: Discussionmentioning

confidence: 99%

“…25 Heparin was also found to inhibit the nuclear factor kappa B (NF-κ≡) pathway in monocytes treated with LPS. 26 27 Furthermore, data recently obtained by our group showed that after LPS injury in human alveolar macrophages heparin limited the expression of TNF-α and IL-6, while in human alveolar type II cells heparin inhibited the NF-κ≡ pathway and their effectors IL-6, MCP-1 and IL-8. 28…”

Section: Introductionmentioning

confidence: 91%

Nebulized Heparin Attenuates Pulmonary Coagulopathy and Inflammation through Alveolar Macrophages in a Rat Model of Acute Lung Injury

et al. 2017

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Objective Alveolar macrophages play a key role in the development and resolution of acute respiratory distress syndrome (ARDS), modulating the inflammatory response and the coagulation cascade in lungs. Anti-coagulants may be helpful in the treatment of ARDS. This study investigated the effects of nebulized heparin on the role of alveolar macrophages in limiting lung coagulation and inflammatory response in an animal model of acute lung injury (ALI). Methods Rats were randomized to four experimental groups. In three groups, ALI was induced by intratracheal instillation of lipopolysaccharide (LPS) and heparin was nebulized at constant oxygen flow: the LPS/Hep group received nebulized heparin 4 and 8 hours after injury; the Hep/LPS/Hep group received nebulized heparin 30 minutes before and 4 and 8 hours after LPS-induced injury; the LPS/Sal group received nebulized saline 4 and 8 hours after injury. The control group received only saline. Animals were exsanguinated 24 hours after LPS instillation. Lung tissue, bronchoalveolar lavage fluid (BALF) and alveolar macrophages isolated from BALF were analysed. Results LPS increased protein concentration, oedema and neutrophils in BALF as well as procoagulant and proinflammatory mediators in lung tissue and alveolar macrophages. In lung tissue, nebulized heparin attenuated ALI through decreasing procoagulant (tissue factor, thrombin-anti-thrombin complexes, fibrin degradation products) and proinflammatory (interleukin 6, tumour necrosis factor alpha) pathways. In alveolar macrophages, nebulized heparin reduced expression of procoagulant genes and the effectors of transforming growth factor beta (Smad 2, Smad 3) and nuclear factor kappa B (p-selectin, CCL-2). Pre-treatment resulted in more pronounced attenuation. Conclusion Nebulized heparin reduced pulmonary coagulopathy and inflammation without producing systemic bleeding, partly by modulating alveolar macrophages.

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“…In addition, O-desulfated heparin prevented dysfunction of endothelialdependent coronary relaxation following ischemic injury and inhibited translocation of the proinflammatory transcription nuclear factor-jB (NF-jB) from the cytoplasm to the nucleus in human endothelial cells and decreased NF-jB DNA binding in human endothelium and ischemic-reperfused rat myocardium [16]. Recently, fucan and dextran derivatives and heparin were found to modulate, in a dose-dependent manner, the release of proinflammatory cytokines by resting or LPSstimulated human monocytes and to interact with monocyte surfaces by inhibiting LPS-binding to monocyte membranes [17].…”

Section: Introductionmentioning

confidence: 99%

Cytokine gene expression and production by human LPS‐stimulated mononuclear cells are inhibited by sulfated heparin‐like semi‐synthetic derivatives

Gori

Attanasio

Gazzini

et al. 2004

Journal of Thrombosis and Haemostasis

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Summary. Background: The K5 polysaccharide obtained from Escherichia coli strain 010:K5:H4 is a polymer of the disaccharidic unit formed by D-glucuronic acid and Nacetylglucosamine. This structure is akin to N-acetylheparosan, the precursory polymer of heparin and of heparan sulfate. This structural affinity with N-acetylated heparin and with desulfated heparin makes the K5 polysaccharide extremely useful for the preparation of sulfated heparin-like semi-synthetic derivatives. It has been demonstrated that heparins are able to inhibit tissue factor and cytokine production and expression by human monocytes. Objective: The aim of this study was to evaluate the effects of four different heparin-like semi-synthetic derivatives on inflammatory cytokine production and expression by human mononuclear cells. Results: The simultaneous addition of lipopolysaccharide (LPS; 0.2 and 10 lg mL ), K5-OS or K5-N, OS epi at 5 and 10 lg mL )1 markedly decreased TNF-a mRNA expression. Conclusions: These results indicate that the sulfated heparin-like semi-synthetic derivatives K5-OS and K5-N, OS epi are able to inhibit both expression and production of inflammatory cytokines, whereas they do not influence the anti-inflammatory cytokine IL-10, suggesting a potential role for these products as modulators of inflammatory reactions.

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Heparin‐like polymers modulate proinflammatory cytokine production by lipopolysaccharide‐stimulated human monocytes

Cited by 19 publications

References 50 publications

Evaluation of Anti-Nociceptive and Anti-Inflammatory Activities of a Heterofucan from Dictyota menstrualis

Evaluation of Anti-Nociceptive and Anti-Inflammatory Activities of a Heterofucan from Dictyota menstrualis

Nebulized Heparin Attenuates Pulmonary Coagulopathy and Inflammation through Alveolar Macrophages in a Rat Model of Acute Lung Injury

Cytokine gene expression and production by human LPS‐stimulated mononuclear cells are inhibited by sulfated heparin‐like semi‐synthetic derivatives

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