RESUMEN
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-1ß, 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-1ß 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.
Asunto(s)
Antiinflamatorios/administración & dosificación , Colitis/terapia , Sinergismo Farmacológico , Limosilactobacillus reuteri/crecimiento & desarrollo , Aceites/administración & dosificación , Probióticos/administración & dosificación , Vitamina D/administración & dosificación , Animales , Antiinflamatorios/farmacología , Adhesión Bacteriana , Peso Corporal , Línea Celular , Colitis/inducido químicamente , Colitis/patología , Citocinas/análisis , Sulfato de Dextran/administración & dosificación , Sulfato de Dextran/toxicidad , Modelos Animales de Enfermedad , Euphausiacea , Histocitoquímica , Humanos , Ratones Endogámicos C57BL , Modelos Biológicos , Aceites/farmacología , Probióticos/farmacología , Resultado del Tratamiento , Vitamina D/farmacologíaRESUMEN
Inspite of increased technical difficulties and high incidence of conversion to open procedures and complications, laparoscopic cholecystectomy is a well established treatment for acute cholecystitis. In this study we reported our results in patients with acute cholecystitis undergoing laparoscopic cholecystecomy from 1998 to 2003. We found out that laparoscopic cholecystectomy was safe and was carried out with acceptable conversion rate and low morbidity. Predictors of complications were delay of surgery more than 48 hours following the onset of symptoms, leucocytosis > 15.000 U/microl and gallbladder wall ultrasonography thickness > 7mm.