fucoidin/inflammation

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The polysaccharide fucoidin inhibits the antibiotic-induced inflammatory cascade in experimental pneumococcal meningitis.

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There is evidence that the treatment of bacterial meningitis with antibiotics liberates harmful bacterial products in the subarachnoid space (SAS). This enhances meningeal inflammation and in particular the recruitment of leukocytes into the cerebrospinal fluid (CSF), which has been shown to be more

Fucoidin, a polysaccharide inhibiting leukocyte rolling, attenuates inflammatory responses in experimental pneumococcal meningitis in rats.

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It is presumed that adjuvant therapy rather than new antibiotics will improve the prognosis of pneumococcal meningitis. We investigated the effect of fucoidin, a polysaccharide inhibiting leukocyte rolling, on inflammatory changes in experimental meningitis in rats. After induction of meningitis by

Fucoidin, a potent inhibitor of leukocyte rolling, prevents neutrophil influx into phorbol-ester-induced inflammatory sites in rabbit lungs.

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The polysaccharide fucoidin, a homopolymer of sulfated L-fucose, is known, by interfering with the function of L-selectin, to inhibit leukocyte rolling, which is an early and essential step in the process of leukocyte extravasation into inflamed sites. We tested the inhibitory effect of fucoidin on

Cooperative role of tumour necrosis factor-α, interleukin-1β and neutrophils in a novel behavioural model that concomitantly demonstrates articular inflammation and hypernociception in mice.

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BACKGROUND AND PURPOSE; Chronic joint inflammation and pain are the hallmarks of disease in patients with inflammatory arthritis, notably rheumatoid arthritis. The aim of the present study was to investigate the relative contribution of tumour necrosis factor (TNF)-α, interleukin (IL)-1β and

Inhibition of leukocyte rolling with polysaccharide fucoidin prevents pleocytosis in experimental meningitis in the rabbit.

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Inflammatory recruitment of leukocytes into the cerebrospinal fluid (CSF) during bacterial meningitis has been shown to contribute significantly to the neurological damage commonly associated with this serious disease. In this study we tested whether or not inhibition of leukocyte rolling, a

IL-33/ST2 signalling contributes to carrageenin-induced innate inflammation and inflammatory pain: role of cytokines, endothelin-1 and prostaglandin E2.

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OBJECTIVE IL-33 signals through ST2 receptors and induces adaptive and innate inflammation. IL-33/ST2 is involved in adaptive inflammation-induced pain. Here, we have investigated the contribution of IL-33/ST2-triggered mechanisms to carrageenin-induced innate inflammation. METHODS Carrageenin- and

Effects of polysaccharide fucoidin on cerebrospinal fluid interleukin-1 and tumor necrosis factor alpha in pneumococcal meningitis in the rabbit.

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The inflammatory response in bacterial meningitis is mediated by cytokines, such as tumor necrosis factor alpha (TNF-alpha) and interleukin-1 (IL-1), which are produced in the subarachnoid space by different cells, e.g., leukocytes, astrocytes, and microglia. The recruitment of leukocytes into the

Neuroprotective effect of fucoidin on lipopolysaccharide accelerated cerebral ischemic injury through inhibition of cytokine expression and neutrophil infiltration.

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In our previous study, we reported that lipopolysaccharide (LPS) activated microglia and accelerated cerebral ischemic injury in the rat brain through the overexpression of cytokines in microglia. In the present study, we investigated the effect of the intraperitoneal administration of fucoidin, a

Selectins and integrins but not platelet-endothelial cell adhesion molecule-1 regulate opioid inhibition of inflammatory pain.

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1. Control of inflammatory pain can result from activation of opioid receptors on peripheral sensory nerves by opioid peptides secreted from leukocytes in response to stress (e.g. experimental swim stress or surgery). The extravasation of immunocytes to injured tissues involves rolling, adhesion and

Fucoidin prevents Clostridium difficile toxin-A-induced ileal enteritis in mice.

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Recent reports suggest increased incidence and severity of Clostridium difficile-associated diseases. These facts have raised the need for additional clarification of pathogenesis and for a search for new therapeutic strategies. This study evaluated the effects of the polysaccharide fucoidin, an

Light-emitting diode therapy reduces persistent inflammatory pain: Role of interleukin 10 and antioxidant enzymes.

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BACKGROUND During the last decades, the use of light-emitting diode therapy (LEDT) has increased significantly for the treatment of wound healing, analgesia and inflammatory processes. Nevertheless, scientific data on the mechanisms responsible for the therapeutic effect of LEDT are still

Relief of inflammatory pain in rats by local use of the selective P2X7 ATP receptor inhibitor, oxidized ATP.

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OBJECTIVE Oxidized ATP (oATP) is a selective inhibitor of the P2Z/P2X7 ATP receptor for extracellular ATP, which contributes to the antinociceptive effect. This study sought to determine the mechanism by which local administration of oATP is able to relieve inflammatory pain in arthritic rat

The effect of the selectin binding polysaccharide fucoidin on eosinophil recruitment in vivo.

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1. In order to accumulate at sites of inflammation, leukocytes initially roll on endothelial cells of postcapillary venules before becoming firmly attached. This process of rolling is mediated by selectins which bind to carbohydrate counter-ligands present on the surface of both leukocytes and

Crucial role of neutrophils in the development of mechanical inflammatory hypernociception.

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Neutrophil migration is responsible for tissue damage observed in inflammatory diseases. Neutrophils are also implicated in inflammatory nociception, but mechanisms of their participation have not been elucidated. In the present study, we addressed these mechanisms in the carrageenan-induced

Platelet abnormalities during colonic inflammation.

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Patients with inflammatory bowel disease are susceptible to microvascular thrombosis and thromboembolism. The increased incidence of thrombosis is accompanied by enhanced coagulation and abnormalities in platelet function. Clinical studies have revealed thrombocytosis, alterations in platelet

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