Publications by authors named "Anouk Kaulmann"

Due to their anti-oxidant and anti-inflammatory potential, polyphenol and carotenoid-rich plant foods have been suggested as promising phytochemicals in the prevention of or as adjuvants regarding inflammatory bowel diseases (IBD). In the present study, we investigated whether plum (Italian Plum, Prunus cocomilla), or cabbage (Kale, Brassica oleracea var. sabellica), selected for their high phytochemical content, are able to reduce inflammation in cellular models of the intestinal epithelium, employing proteomic methods.

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Inflammatory bowel diseases (IBDs) are characterized by autoimmune and inflammation-related complications of the large intestine (ulcerative colitis) and additional parts of the digestive tract (Crohn's disease). Complications include pain, diarrhoea, chronic inflammation, and cancer. IBD prevalence has increased during the past decades, especially in Westernized countries, being as high as 1%.

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Scope: Plums/cabbages represent fruits/vegetables rich in carotenoids and polyphenols, and have been associated with anti-inflammatory properties.

Methods And Results: We tested four plum (Italian Plum, Plum 620, Ersinger, and Cherry Plum) and cabbage varieties (Duchy, Kalorama, Kale, Scots Kale) with contrasting carotenoid/polyphenol content for their capability to alter inflammation/oxidative stress following simulated gastrointestinal digestion. Digesta were exposed to Caco-2(TC-7) and to a triple-culture(Caco-2/HT-29-MTX (90:10 v/v) including THP-1 like macrophages), stimulated to induce inflammation (10 μg/mL LPS, 100 ng/mL TNF-α, 25 ng/mL IL-1-β for 24 h, the last 18 h with digesta).

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Plum and cabbage are rich in carotenoids and polyphenols. However, their bioactivity depends on their release and intestinal uptake. Four varieties of Brassicaceae (Duchy, Scots Kale, Kale, Kalorama) and Prunus (Cherry Plum, Plum 620, Ersinger, Italian Plum) were studied; bioaccessibility following in vitro digestion, cellular uptake (Caco-2 vs.

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The impact of microwave (1000 W - 340 s) and conventional heat (97 °C - 30s) pasteurisation and storage (4, 10, 22 °C for up to 63 d) on total and individual carotenoids and chlorophylls in kiwifruit puree was evaluated. Bioaccessibility of carotenoids, before and after pasteurisation and storage, was also studied. Microwaves and conventional heating led to marked changes in the chlorophyll (42-100% losses) and carotenoid (62-91% losses) content.

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Several epidemiologic studies have shown that diets rich in fruits and vegetables reduce the risk of developing several chronic diseases, such as type 2 diabetes, atherosclerosis, and cancer. These diseases are linked with systemic, low-grade chronic inflammation. Although controversy persists on the bioactive ingredients, several secondary plant metabolites have been associated with these beneficial health effects.

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The consumption of phytochemicals such as carotenoids and polyphenols within whole fruits and vegetables has been associated with decreased incidence of various inflammation and oxidative stress related chronic diseases, which may be due to direct antioxidant effects, or indirect mechanisms such as affecting signal transduction/gene expression. Within the present study, we investigated the antioxidant composition of two major groups of vegetables and fruits, Brassica oleraceae and prunus spp., and estimated their contribution to antioxidant capacity.

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Carotenoid consumption has been linked to a number of beneficial health effects, including the reduction of chronic diseases such as cancer and cardiovascular complications. However, no data are available on their action on the intestinal epithelium, being exposed to the highest concentrations of carotenoids in the human body, and where they could act preventively on intestinal inflammatory diseases such as Crohn's disease and ulcerative colitis. The objective of the present study was to investigate whether lycopene and β-carotene in micelles (M), at concentrations that could be reached via the diet (10-25 μg/ml) could aid in the reduction of TNF-α plus IL-1β-induced inflammation of Caco-2 human epithelial cells.

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