Immune modulation by chondroitin sulfate and its degraded disaccharide product in the development of an experimental model of multiple sclerosis

Zhou, Juhua; Nagarkatti, Mitzi; Yin, Zhimin; Nagarkatti, Mitzi

doi:10.1016/j.jneuroim.2010.04.002

Cited by 42 publications

(35 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Additionally, Zhou and his group have reported on the immune modulation by the animal model of experimental autoimmune encephalomyelitis (EAE) using CS and its disaccharide. It was shown that CS-A and disaccharide degradation of CSPG had an opposite effect on EAE [40]. Thus, it is suggested that CS has different immunochemical reactivity due to its structural variation.…”

Section: Discussionmentioning

confidence: 99%

Effect of Molecular Sizes of Chondroitin Sulfate on Interaction with L-Selectin

Igarashi

Takeguchi

Sakai

et al. 2013

International Journal of Carbohydrate Chemistry

View full text Add to dashboard Cite

Chondroitin sulfate (CS) is a glycosaminoglycan (GAG) side chain of proteoglycans (PGs) which are widely distributed in the extracellular matrix and at cell surface. CS shows a highly structural diversity in not only molecular weight (MW) but sulfonation pattern. CS has been reported to exert anti-inflammatory activity by having effects on cytokine production by helper T cells. In this study, we focused on the structures of CS chains, especially MW of CS, and investigated effect of the different MW of CS on binding affinity with L-selectin and cytokine production by murine splenocytes. Firstly, we fractionated CS by employing gel filtration chromatography and obtained several CS fractions with different MW. Then the interaction between fractionated CS and L-selectin was analyzed by surface plasmon resonance (SPR). Finally, the influence of MW of CS on cytokine production by murine splenocytes was investigated in vitro. The results showed that interferon-gamma production was significantly increased by mouse splenocytes cocultivated with CS. On the contrary, CS inhibited interleukin 5 production by murine splenocytes depending on MW of the cocultivated CS. These results strongly indicate the existence of the optimal molecular size for an anti-inflammatory effect of CS through cytokine production by murine splenocytes.

show abstract

Section: Discussionmentioning

confidence: 99%

Effect of Molecular Sizes of Chondroitin Sulfate on Interaction with L-Selectin

Igarashi

Takeguchi

Sakai

et al. 2013

International Journal of Carbohydrate Chemistry

View full text Add to dashboard Cite

show abstract

“…Data were presented as mean ± SEM. The Wilcoxon rank-sum test was used in statistical analysis as described previously [14], and. Pearson’s correlation test was used to determine the association between cytokine expression and sepsis severity.…”

Section: Methodsmentioning

confidence: 99%

Dysregulation in microRNA expression in peripheral blood mononuclear cells of sepsis patients is associated with immunopathology

et al. 2015

Self Cite

View full text Add to dashboard Cite

Sepsis is a major cause of death worldwide. It triggers systemic inflammation, the role of which remains unclear. In the current study, we investigated the induction of microRNA (miRNA) during sepsis and their role in the regulation of inflammation. Patients, on days 1 and 5 following sepsis diagnosis, had reduced T cells but elevated monocytes. Plasma levels of IL-6, IL-8, IL-10 and MCP-1 dramatically increased in sepsis patients on day 1. T cells from sepsis patients differentiated primarily into Th2 cells, whereas regulatory T cells decreased. Analysis of 1163 miRNAs from PBMCs revealed that miR-182, miR-143, miR-145, miR-146a, miR-150, and miR-155 were dysregulated in sepsis patients. miR-146a downregulation correlated with increased IL-6 expression and monocyte proliferation. Bioinformatics analysis uncovered the immunological associations of dysregulated miRNAs with clinical disease. The current study demonstrates that miRNA dysregulation correlates with clinical manifestations and inflammation, and therefore remains a potential therapeutic target against sepsis.

show abstract

“…Improved recovery was associated with decreased T-cell infiltration and activation (Rolls et al, 2006). In contrast, intravenous administration of intact CS-A prior to EAE symptom onset was detrimental for EAE progression, possibly by driving activation of T-cells towards EAE-propagating Th1 and Th17 cells (Zhou et al, 2010). Therefore, in EAE models, the balance between intact CS-A and its degradation product CSPG-DS have crucial implications for the intensity and duration of inflammation (for review, see (Haylock-Jacobs et al, 2011).…”

Section: Sulfated Proteoglycansmentioning

confidence: 99%

Extracellular matrix regulation of inflammation in the healthy and injured spinal cord

Gaudet

Popovich

2014

Experimental Neurology

179

133

View full text Add to dashboard Cite

Throughout the body, the extracellular matrix (ECM) provides structure and organization to tissues and also helps regulate cell migration and intercellular communication. In the injured spinal cord (or brain), changes in the composition and structure of the ECM undoubtedly contribute to regeneration failure. Less appreciated is how the native and injured ECM influences intraspinal inflammation and, conversely, how neuroinflammation affects the synthesis and deposition of ECM after CNS injury. In all tissues, inflammation can be initiated and propagated by ECM disruption. Molecules of ECM newly liberated by injury or inflammation include hyaluronan fragments, tenascins, and sulfated proteoglycans. These act as “damage-associated molecular patterns” or “alarmins”, i.e., endogenous proteins that trigger and subsequently amplify inflammation. Activated inflammatory cells, in turn, further damage the ECM by releasing degradative enzymes including matrix metalloproteinases (MMPs). After spinal cord injury (SCI), destabilization or alteration of the structural and chemical composition of the ECM affects migration, communication, and survival of all cells – neural and non-neural – that are critical for spinal cord repair. By stabilizing ECM structure or modifying their ability to trigger the degradative effects of inflammation, it may be possible to create an environment that is more conducive to tissue repair and axon plasticity after SCI.

show abstract

Immune modulation by chondroitin sulfate and its degraded disaccharide product in the development of an experimental model of multiple sclerosis

Cited by 42 publications

References 47 publications

Effect of Molecular Sizes of Chondroitin Sulfate on Interaction with L-Selectin

Effect of Molecular Sizes of Chondroitin Sulfate on Interaction with L-Selectin

Dysregulation in microRNA expression in peripheral blood mononuclear cells of sepsis patients is associated with immunopathology

Extracellular matrix regulation of inflammation in the healthy and injured spinal cord

Contact Info

Product

Resources

About