Chitosan oligosaccharides suppressant LPS binding to TLR4/MD-2 receptor complex

Qiao, Ying; Ruan, Yuanyuan; Xiong, Chao; Xu, Qingsong; Wei, Peng; Ma, Pan; X, Bai; Du, Yuguang

doi:10.1016/j.carbpol.2010.04.079

Cited by 37 publications

(27 citation statements)

References 43 publications

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“…This latter outcome is not completely unexpected. Qiao et al (2010) reported that chitosan oligosaccharides could suppress LPS binding to TLR4/MD-2 receptor complexes, thereby attenuating activation of mitogenactivated protein kinases (MAPKs) and leading to decreased nuclear translocation of nuclear factor-B (NF-B). Those authors concluded that chitosan oligosaccharides could in fact serve as potential inhibitors of LPS-inducible release of proinflammatory mediators like IL-1 and nitric oxide (NO) from macrophages.…”

Section: Discussionmentioning

confidence: 99%

Effects of 3-dimensional culture conditions (collagen-chitosan nano-scaffolds) on maturation of dendritic cells and their capacity to interact with T-lymphocytes

Daneshmandi

Dibazar

Fateh

2015

Journal of Immunotoxicology

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In the body, there is a natural three-dimensional (3D) microenvironment in which immune cells, including dendritic cells (DC), play their functions. This study evaluated the impact of using collagen-chitosan 3D nano-scaffolds in comparisons to routine 2D culture plates on DC phenotype and functions. Bone marrow-derived DC were cultured on scaffolds and plates and then stimulated with lipopolysaccharide (LPS) or chitosan-based nanoparticles (NP) for 24 h. Thereafter, DC viability, expression of maturation markers and levels of cytokines secretion were evaluated. In another set of studies, the DC were co-cultured with allogenic T-lymphocytes in both the 2D and 3D systems and effects on DC-induction of T-lymphocyte proliferation and cytokine release were analyzed. The results indicated that CD40, CD86 and MHC II marker expression and interleukin (IL)-12, IL-6 and tumor necrosis factor (TNF)-secretion by DC were enhanced in 3D cultures in comparison to by cells maintained in the 2D states. The data also showed that DNA/chitosan NP activated DC more than LPS in the 3D system. T-Lymphocyte proliferation was induced to a greater extent by DNA/NP-treated DC when both cell types were maintained on the scaffolds. Interestingly, while DC induction of T-lymphocyte interferon (IFN)-and IL-4 release was enhanced in the 3D system (relative to controls), there was a suppression of transforming growth factor (TGF)-production; effects on IL-10 secretion were variable. The results here suggested that collagen-chitosan scaffolds could provide a proinflammatory and activator environment to perform studies to analyze effects of exogenous agents on the induction of DC maturation, NP uptake and/or cytokines release, as well as for the ability of these cells to potentially interact with other immune system cells in vitro.

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Section: Discussionmentioning

confidence: 99%

Effects of 3-dimensional culture conditions (collagen-chitosan nano-scaffolds) on maturation of dendritic cells and their capacity to interact with T-lymphocytes

Daneshmandi

Dibazar

Fateh

2015

Journal of Immunotoxicology

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“…The evolutionary conserved family of mitogen-activated protein kinases (MAPKs) includes extracellular p38 MAPK, extracellular regulated protein kinase (ERK) and c-Jun N-terminal kinase (JNK) (15). Numerous environmental stresses, such as osmotic shock, ultraviolet irradiation, as well as LPS and pro-inflammatory cytokines, have been confirmed to activate MAPK signaling cascades in a variety of cell lines (11,16).…”

Section: Introductionmentioning

confidence: 99%

Chitosan oligosaccharides downregulate the expression of E-selectin and ICAM-1 induced by LPS in endothelial cells by inhibiting MAP kinase signaling

Liu

Wei

et al. 2013

International Journal of Molecular Medicine

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Abstract. The expression of adhesion molecules in endothelial cells elicited by lipopolysaccharide (LPS) is involved in the adhesive interaction between endothelial cells and monocytes in inflammation. In this study, in order to characterize the anti-inflammatory effects of chitosan oligosaccharides (COS) on LPS-induced inflammation and to elucidate the underlying mechanisms, the mRNA levels of E-selectin and intercellular adhesion molecule-1 (ICAM-1) were measured in porcine iliac artery endothelial cells (PIECs). When these cells were treated with COS, the LPS-induced mRNA expression of E-selectin and ICAM-1 was reduced through the inhibition of the signal transduction cascade, p38 mitogen-activated protein kinase (MAPK)/extracellular regulated protein kinase 1/2 (ERK1/2) and nuclear factor-κB (NF-κB). Moreover, through the inhibition of p38 MAPK and ERK1/2, COS suppressed the LPS-induced NF-κB p65 translocation. We found that COS suppressed the phosphorylation of p38 MAPK and the translocation of NF-κB p65 into the nucleus in a dose-dependent manner, and inhibited the adhesion of U973 cells to PIECs. Based on these results, it can be concluded that COS downregulate the expression of E-selectin and ICAM-1 by inhibiting the phosphorylation of MAPKs and the activation of NF-κB in LPS-treated PIECs. Our study demonstrates the valuable anti-inflammatory properties of COS. IntroductionChitosan oligosaccharides (COS), consisting of D-glucosamine linked via β-1,4-glycosides, are derived from chitosan by chemical or enzymatic hydrolysis (1). It has been reported that COS exhibit various biological activities, such as antitumor (2) and antioxidant properties (3), owing to their low molecular weight, high absorption, solubility and biocompatibility (4). In addition, recent studies have paid more attention to the regulatory role of COS in inflammatory responses (5,6).Lipopolysaccharide (LPS), the major component of the outer membrane of Gram-negative bacteria, can act as an endotoxin and initiates serious inflammatory responses in vitro and in vivo (7,8) by upregulating the expression of adhesion molecules and cytokines, such as E-selectin, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and tumor necrosis factor-α (TNF-α) (9,10). Endothelial cells are the target of inflammatory responses and thereby, of a number of severe disorders, including sepsis and multiple organ dysfunctions that occur via LPS stimulation (11). In this study, we detected the expression of the adhesion molecules, E-selectin and ICAM-1 in LPS-treated porcine iliac artery endothelial cells (PIECs), since the upregulation of adhesion molecules and the increased secretion of cytokines and chemokines are known to occur during endothelial cell activation (12)(13)(14).The evolutionary conserved family of mitogen-activated protein kinases (MAPKs) includes extracellular p38 MAPK, extracellular regulated protein kinase (ERK) and c-Jun N-terminal kinase (JNK) (15). Numerous environmental stresses, such as osmotic shock, ...

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“…It warrants further investigation on how COS modulate the complex crosstalk among MAPK, superoxide, and OGT to exert its anti-inflammatory function. It is worth noting that as a logical extension to the published studies, the present paper focused only on intracellular effects of COS; however, it does not exclude the extracellular impacts from COS as found in cultured immune cells (Qiao et al, 2010). It also merits further investigation on the role of COS in not only the prevention but also the treatment of inflammation.…”

Section: Discussionmentioning

confidence: 99%

Chitosan oligosaccharides block LPS-induced O-GlcNAcylation of NF-κB and endothelial inflammatory response

Liu

et al. 2014

Carbohydrate Polymers

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It is known that chitosan oligosaccharides (COS) suppress LPS-induced vascular endothelial inflammatory response by mechanism involving NF-κB blockade. It remains unknown how COS inhibit NF-κB. We provided evidence both in cultured endothelial cells and mouse model supporting a new mechanism. Regardless of the endothelial cell types, the LPS-induced NF-κB-dependent inflammatory gene expression was suppressed by COS, which was associated with reduced NF-κB nucleus translocation. LPS enhanced O-GlcNAc modification of NF-κB/p65 and activated NF-κB pathway, which could be prevented either by siRNA knockdown of O-GlcNAc transferase (OGT) or pretreatment with COS. Inhibition of either mitogen-activated protein kinase or superoxide generation abolishes LPS-induced NF-κB O-GlcNAcylation. Consistently, aortic tissues from LPS-treated mice presented enhanced NF-κB/p65 O-GlcNAcylation in association with upregulated gene expression of inflammatory cytokines in vascular tissues; however, pre-administration of COS prevented these responses. In conclusion, COS decreased OGT-dependent O-GlcNAcylation of NF-κB and thereby attenuated LPS-induced vascular endothelial inflammatory response.

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Chitosan oligosaccharides suppressant LPS binding to TLR4/MD-2 receptor complex

Cited by 37 publications

References 43 publications

Effects of 3-dimensional culture conditions (collagen-chitosan nano-scaffolds) on maturation of dendritic cells and their capacity to interact with T-lymphocytes

Effects of 3-dimensional culture conditions (collagen-chitosan nano-scaffolds) on maturation of dendritic cells and their capacity to interact with T-lymphocytes

Chitosan oligosaccharides downregulate the expression of E-selectin and ICAM-1 induced by LPS in endothelial cells by inhibiting MAP kinase signaling

Chitosan oligosaccharides block LPS-induced O-GlcNAcylation of NF-κB and endothelial inflammatory response

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