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Dietary supplementation with laminarin, a fermentable marine beta (1-3) glucan, protects against hepatotoxicity induced by LPS in rat by modulating immune response in the hepatic tissue Neyrinck, A.; Mouson, A.; Delzenne, N.M. (2007). Dietary supplementation with laminarin, a fermentable marine beta (1-3) glucan, protects against hepatotoxicity induced by LPS in rat by modulating immune response in the hepatic tissue. Int. Immunopharmacol. 7(12): 1497-1506. http://dx.doi.org/10.1016/j.intimp.2007.06.011 In: International Immunopharmacology. Elsevier: Amsterdam. ISSN 1567-5769; e-ISSN 1878-1705 Is gerelateerd aan: Neyrinck, A.; Mouson, A.; Delzenne, N.M. (2008). Response to "Comment on: Dietary supplementation with laminarin, a fermentable marine beta (1-3) glucan, protects against hepatotoxicity induced by LPS in rat by modulating immune response in the hepatic tissue". Int. Immunopharmacol. 8(3): 516-517. dx.doi.org/10.1016/j.intimp.2007.12.001, meer Is gerelateerd aan: Chen, J. (2008). Comment on: Dietary supplementation with laminarin, a fermentable marine beta (1-3) glucan, protects against hepatotoxicity induced by LPS in rat by modulating immune response in the hepatic tissue. Int. Immunopharmacol. 8(3): 514-515. http://dx.doi.org/10.1016/j.intimp.2007.12.002, meer

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Beschikbaar in	Auteurs
VLIZ: Open Marine Archive 292134 [ download pdf ]

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Trefwoord

Marien/Kust

Author keywords

Kupffer cells; ß-glucan; Laminarin; LPS

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Auteurs		Top
Neyrinck, A. Mouson, A. Delzenne, N.M.

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Abstract

We tested the hypothesis that laminarin (LAM), a ß (1–3) polysaccharide extracted from brown algae, can modulate the response to a systemic inflammation. Male Wistar rats (n = 7 per group) were fed a standard diet (control) or a diet supplemented with LAM for 25 days (5% during 4 days followed by 10% during 21 days). Thereafter, Escherichia coli lipopolysaccharides (LPS; 10 mg/kg i.p.) were injected and the animals were sacrificed 24 h after LPS challenge. The hypothermia, hyperglycemia and hypertriglyceridemia occurring early after LPS administration were less pronounced in LAM-treated rats than in controls. The increase in serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) activities – reflecting hepatic alterations – was lessened after LPS injection in LAM-treated rats compared to control rats. LAM treatment decreased serum monocytes number, nitrite (NO2) and tumor necrosis factor-alpha (TNF-a). LAM also modulated intra-hepatic immune cells: it lowered the occurrence of peroxidase-positive cells (corresponding to monocytes/neutrophils) and, in contrast, it increased the number of ED2-positive cells, corresponding to resident hepatic macrophages, i.e. Kupffer cells. In conclusion, the hepatoprotective effect of marine ß (1–3) glucan during endotoxic shock may be linked to its immunomodulatory properties. We propose that both lower recruitment of inflammatory cells inside the liver tissue and lower secretion of inflammatory mediators play a role in the tissue protective effect of LAM. These effects could be due to a direct effect of ß-glucan on immune cells, or to an indirect effect through their dietary fibre properties (fermentation in the gut).

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