Menchetti Laura, Curone Giulio, Filipescu Iulia Elena, Barbato Olimpia, Leonardi Leonardo, Guelfi Gabriella, Traina Giovanna, Casagrande-Proietti Patrizia, Riva Federica, Casano Anna Beatrice, Piro Federica, Vigo Daniele, Quattrone Alda, Brecchia Gabriele
Department of Veterinary Medicine, University of Perugia, Via San Costanzo 4, 06126 Perugia, Italy.
Department of Veterinary Medicine, University of Milano, Via dell'Università 6, 26900 Lodi, Italy.
Animals (Basel). 2020 Mar 15;10(3):492. doi: 10.3390/ani10030492.
This study investigated the effects of a short-term administration of bovine colostrum (BC) in a TNBS model of induced colitis. Colitis was induced by TNBS treatment after seven days of BC (BC group, n = 12) or saline (control group, n = 12) administration in mice. Clinical signs, histopathological characteristics, expression levels of Toll-like receptor 4 (TLR4), pro- and anti-inflammatory cytokines, and microbial composition were assessed. BC was well tolerated and did not induce any histological damage or clinical symptoms. After TNBS treatment, the BC group showed a reduction in body weight (BW) loss compared to Control ( < 0.05). Moreover, expression levels of TLR4 ( < 0.01), Interleukin-1β (IL-1β; < 0.001), Interleukin-8 (IL-8; < 0.001), and Interleukin-10 (IL-10; < 0.001) were lower in mice administered with BC. Finally, were higher ( < 0.05), while Enterococci ( < 0.001), spp. ( < 0.001), and spp. ( < 0.05) were lower in Control than BC group. This study confirms that pre-treatment with BC modulates the expression of genes and the count of microbes involved in the etiopathogenesis of colitis.
本研究调查了在三硝基苯磺酸（TNBS）诱导的结肠炎模型中短期给予牛初乳（BC）的效果。在小鼠中给予BC（BC组，n = 12）或生理盐水（对照组，n = 12）7天后，通过TNBS处理诱导结肠炎。评估了临床体征、组织病理学特征、Toll样受体4（TLR4）的表达水平、促炎和抗炎细胞因子以及微生物组成。BC耐受性良好，未引起任何组织学损伤或临床症状。TNBS处理后，与对照组相比，BC组体重（BW）损失减少（<0.05）。此外，给予BC的小鼠中TLR4（<0.01）、白细胞介素-1β（IL-1β；<0.001）、白细胞介素-8（IL-8；<0.001）和白细胞介素-10（IL-10；<0.001）的表达水平较低。最后，对照组中[此处原文缺失相关内容]较高（<0.05），而肠球菌（<0.001）、[此处原文缺失相关菌属名称]菌属（<0.001）和[此处原文缺失相关菌属名称]菌属（<0.05）低于BC组。本研究证实，BC预处理可调节参与结肠炎发病机制的基因表达和微生物数量。
