In vitro experiments have demonstrated that polyphenols exhibit antioxidant and anti-inflammatory activities. The present study was designed to test whether dealcoholized red (DRW) and white (DWW) wines can decrease the oxidative stress associated with inflammation in vivo. Rats were fed for 15 d either a control diet or one supplemented with DRW or DWW. Finally, a granuloma was induced by subcutaneous administration of carrageenan. Although DRW showed higher antioxidant activity in vitro than DWW, both wines decreased the number of cells recruited into the granuloma pouch. Malondialdehyde decreased in plasma and inflammatory exudate from rats fed with DRW- and DWW-rich diets. Moreover, the concentration of NO increased in exudate, which correlates with the increase in the citrulline:arginine ratio. Polymorphonuclear leucocytes from the inflammatory exudate of rats fed dealcoholized wines showed decreased superoxide anion (O2∙−) production and increased NO production ex vivo. This change in NO production resulted from increased expression and activity of inducible NO synthase (EC 1.14.13.39). Moreover, the up regulation of cyclo-oxygenase-2 (EC 1.14.99.1) protein expression observed in rats fed the DRW-rich diet was not related to a direct effect of NO. The present results indicate that the non-alcoholic compounds of wines not only improve antioxidant status in an inflammatory situation, but also limit cell infiltration, possibly through a decrease in O2∙− and an increase in NO production.

Infection of the cornea with herpes simplex virus (HSV) can result in a chronic disease called herpetic stromal keratitis (HSK). The disease represents one of the leading causes of infectious blindness in the Western world. Immune-mediated cellular damage is suspected in the pathogenesis of human HSK. The murine model has been pivotal in further establishing HSK as an immunopathological disease. This article reviews understanding of HSK, both in humans and in the mouse model, with an emphasis on possible future therapeutic strategies to counteract this blinding immunoinflammatory disease

Recent studies underline the importance of the immunoinflammatory processes in the pathology of Mg deficiency. Neutrophils possess a superoxide anion-generating NADPH oxidase and its inappropriate activation may result in tissue damage. The aim of the present study was to assess the effect of experimental Mg deficiency in the rat on polymorphonuclear leucocytes (PMN) activity and the role of increasing extracellular Mg. Weaning male Wistar rats were fed either a Mg-deficient or a control diet for 8 d. In Mg-deficient rats, the characteristic inflammatory response was accompanied by a marked increase in the number of PMN. Higher plasma interleukin 6 and NO concentrations and increased lipid peroxidation in the heart were found in Mg-deficient rats as compared with control rats. As shown by chemiluminescence studies, basal neutrophil activity from Mg-deficient rats was significantly elevated when compared with neutrophils from control rats. Moreover, the chemiluminescence of PMN from Mg-deficient rats was significantly higher than that of control rats following phorbol myristate acetate or opsonized zymosan activation. PMN from Mg-deficient rats also showed an increased activity of phagocytosis in comparison with neutrophils from control animals. Increasing extracellular Mg concentration in the incubating medium of PMN (0·8 v. 8·0 mM) decreased the chemiluminescence activity of PMN from control rats following opsonized zymosan activation. Chemiluminescence activities of PMN from Mg-deficient rats following phorbol myristate acetate or opsonized zymosan challenge were also decreased by high extracellular Mg concentration. From this work, it appears that PMN activation is an early consequence of Mg deficiency and that high extracellular Mg concentration inhibits free radicals generation.