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Krill oil, vitamin D and Lactobacillus reuteri cooperate to reduce gut inflammation

TitoloKrill oil, vitamin D and Lactobacillus reuteri cooperate to reduce gut inflammation
Tipo di pubblicazioneArticolo su Rivista peer-reviewed
Anno di Pubblicazione2018
AutoriCostanzo, Manuela, Cesi Vincenzo, Palone Francesca, Pierdomenico Maria, Colantoni Eleonora, Leter B, Vitali Roberta, Negroni Anna, Cucchiara S, and Stronati L
RivistaBenef Microbes
Volume9
Issue3
Paginazione389-399
Data di pubblicazione2018 Apr 25
ISSN18762891
Parole chiaveAnimals, Anti-Inflammatory Agents, Bacterial Adhesion, body weight, Cell Line, colitis, Cytokines, Dextran Sulfate, Disease Models, Animal, Drug Synergism, Euphausiacea, Histocytochemistry, Humans, Lactobacillus reuteri, Mice, Inbred C57BL, Models, Biological, Oils, Probiotics, treatment outcome, Vitamin D
Abstract

Current research into original therapies to treat intestinal inflammation is focusing on no-drug therapies. KLD is a mixture of krill oil (KO), probiotic Lactobacillus reuteri (LR), and vitamin D (VitD3). The aim of this study was to assess in vitro and in vivo the potential cooperative effects of KLD in reducing gut inflammation. Colorectal adenocarcinoma cell lines, CACO2 and HT29, and C57BL/6 mice were used for in vitro and in vivo analyses, respectively. Cells were exposed to cytomix (interferon gamma + tumour necrosis factor alpha (TNF-α)) to induce inflammation or co-exposed to cytomix and KO, LR and VitD3 alone or to cytomix and KLD. Animals were treated for 7 days with dextran sodium sulphate (DSS) to induce colitis or with DSS and KLD. In vitro assays: F-actin expression was analysed by immunofluorescence; scratch test and trans-epithelial electric resistance test were performed to measure wound healing; adhesion/invasion assays of adhesive and invasive Escherichia coli (AIEC) bacteria were made; mRNA expression of TNF-α, interleukin (IL)-8 and vitamin D receptor (VDR) was detected by quantitative PCR. In vivo assays: body weight, clinical score, histological score and large intestine weight and length were estimated; mRNA expression of TNF-α, IL-1β, IL-6, IL-10 by quantitative PCR; VDR expression was detected by quantitative PCR and immunohistochemistry. In vitro: KLD restores epithelial cell-cell adhesion and mucosal healing during inflammation, while decreases the adhesiveness and invasiveness of AIEC bacteria and TNF-α and IL-8 mRNA expression and increases VDR expression. In vivo: KLD significantly improves body weight, clinical score, histological score and large intestine length of mice with DSS-induced colitis and reduces TNF-α, IL-1β and IL-6 mRNA levels, while increases IL-10 mRNA and VDR levels. KLD has significant effects on the intestinal mucosa, strongly decreasing inflammation, increasing epithelial restitution and reducing pathogenicity of harmful commensal bacteria.

Note

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URLhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85046806823&doi=10.3920%2fBM2017.0078&partnerID=40&md5=6df17b113fdbdcce3737d09ff99911d6
DOI10.3920/BM2017.0078
Alternate JournalBenef Microbes
Citation Key7061
PubMed ID29633636