首页> 外文期刊>Journal of human lactation: official journal of International Lactation Consultant Association >The Protective Influence of Chondroitin Sulfate, a Component of Human Milk, on Intestinal Bacterial Invasion and Translocation
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The Protective Influence of Chondroitin Sulfate, a Component of Human Milk, on Intestinal Bacterial Invasion and Translocation

机译:软骨素硫酸盐,人乳的组分,肠道细菌侵袭和易位的保护作用

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Background: Human milk is known to be protective against necrotizing enterocolitis, a devastating intestinal inflammatory disease affecting the preterm population. Although the pathogenesis of necrotizing enterocolitis is yet to be solidified, intestinal integrity dysfunction, bacterial invasion and/or translocation, and inflammation may play important roles. Glycosaminoglycans, compounds naturally prevalent in both human milk and the intestine, are thought to be anti-inflammatory and capable of altering bacterial interactions within the gut. Research aim: In this study, we aimed to evaluate the potential of chondroitin sulfate, the most prominent class of glycosaminoglycans in human milk, to protect against bacterial infection in an intestinal in vitro model. Methods: T84 cell monolayers were treated with chondroitin sulfate and cell viability was assessed across a number of doses. Monolayers were then pretreated with chondroitin sulfate and subsequently challenged with E. coli invasion and translocation to evaluate any protective role of the compound against infection. Tight junction barrier function was assessed by transepithelial electrical resistance, and cytokine levels were evaluated. Results: Chondroitin sulfate at any dose up to 750 mu g/ml was not associated with any statistically significant decrease in cell viability. Additionally, chondroitin sulfate at 750 mu g/ml was associated with a 75% decrease in both bacterial invasion and translocation compared to control. Conclusions: These data suggest chondroitin sulfate may protect against bacterial infection through a reduction in both invasion and translocation, importantly without attendant reduction in cell viability.
机译:背景:已知人乳对坏死性小肠结肠炎的保护性,这是一种影响早产的破坏性肠道炎症疾病。虽然坏死性小肠结肠炎的发病机制尚未凝固,肠完整性功能障碍,细菌侵袭和/或易位,并且炎症可能发挥重要作用。糖胺聚糖,在人乳和肠道天然普遍普遍的化合物被认为是抗炎,并且能够改变肠内内的细菌相互作用。研究目标:在这项研究中,我们旨在评估软骨素硫酸盐,最突出的人乳类糖苷类聚糖组的潜力,以防止细菌感染在肠道体外模型中。方法:用软骨素硫酸盐处理T84细胞单层,并在多个剂量上评估细胞活力。然后用硫酸软骨素预处理单层,随后用大肠杆菌侵袭和易位进行攻击,以评估化合物对感染的任何保护作用。通过TRANSEPITHELIAL电阻评估紧密结屏障功能,并评估细胞因子水平。结果:硫酸软骨素在任何剂量上硫酸盐,高达750μmg/ ml与细胞活力的任何统计学上显着的降低无关。另外,与对照相比,硫酸软骨素在750μmg/ ml下与细菌侵袭和易位的降低有关。结论:这些数据表明硫酸软骨素可以通过减少侵袭和易位来保护细菌感染,重要的是没有伴随细胞活力的随附。

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