Bifidobacterial supplementation reduces the incidence of necrotizing enterocolitis in a neonatal rat model
Bifidobacterial supplementation reduces the incidence of necrotizing enterocolitis in a neonatal rat model
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DOI：
10.1016/s0016-5085(99)70450-6
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发表时间：
1999-09-01
期刊：
影响因子：
29.4
通讯作者：
Thomson, R
中科院分区：
文献类型：
--
作者：
Caplan, MS;Miller-Catchpole, R;Thomson, R
背景目的：新生儿坏死性小肠结肠炎（NEC）是早产儿的一种破坏性胃肠道疾病，部分原因是肠道细菌增生。由于双歧杆菌被认为可以降低与致病菌定植相关的肠道紊乱的风险，我们假设向新生大鼠补充外源性双歧杆菌会导致肠道定植并降低新生儿NEC的发病率。方法：新生大鼠幼崽被给予婴儿双歧杆菌（每只动物每天10(9)个有机体）、大肠杆菌或生理盐水对照，并暴露于由配方饲料（Esbilac; 200 cal.kg(-1)）组成的NEC方案。(1))和窒息（100% N-2 50秒，然后冷暴露10分钟）。结局指标包括粪便和肠道微生物学评估、NEC大体和组织学证据、血浆内毒素浓度、肠道磷脂酶A(2)表达和肠粘膜通透性评估。结果：补充双歧杆菌可使肠道定植24小时，粪便样品出现48小时。与对照组和大肠杆菌治疗的动物相比，补充双歧杆菌的动物NEC的发病率显著降低（NEC, 7/24 B.婴儿vs. 19/27对照组vs. 16/23大肠杆菌，）。P < 0.01)。血浆内毒素和肠道磷脂酶A(2)的表达在双歧杆菌处理的幼崽中低于对照组，支持细菌易位和炎症级联激活在NEC病理生理中的作用。结论：肠道双歧杆菌定植可降低新生大鼠NEC的风险。
Background Br Aims: Neonatal necrotizing enterocolitis (NEC) is a devastating gastrointestinal disease of premature infants partly caused by intestinal bacterial proliferation. Because bifidobacteria are thought to reduce the risk for intestinal disturbances associated with pathogenic bacterial colonization, we hypothesized that exogenous bifidobacterial supplementation to newborn rats would result in intestinal colonization and a reduction in the incidence of neonatal NEC. Methods: Newborn rat pups were given Bifidobacterium infantis (10(9) organisms per animal daily), Escherichia coli, or saline control and exposed to the NEC protocol consisting of formula feeding (Esbilac; 200 cal.kg(-1).day(-1)) and asphyxia (100% N-2 for 50 seconds followed by cold exposure for 10 minutes). Outcome measures included stool and intestinal microbiological evaluation, gross and histological evidence of NEC, plasma endotoxin concentration, intestinal phospholipase A(2) expression, and estimation of intestinal mucosal permeability. Results: Bifidobacterial supplementation resulted in intestinal colonization by 24 hours and appearance in stool samples by 48 hours. Bifidobacteria-supplemented animals had a significant reduction in the incidence of NEC compared with controls and E. coli-treated animals (NEC, 7/24 B. infantis vs. 19/27 control vs. 16/23 E. coli,. P < 0.01). Plasma endotoxin and intestinal phospholipase A(2) expression were lower in bifidobacteria-treated pups than in controls, supporting the role of bacterial translocation and activation of the inflammatory cascade in the pathophysiology of NEC. Conclusions: Intestinal bifidobacterial colonization reduces the risk of NEC in newborn rats.