Human milk oligosaccharides shorten rotavirus-induced diarrhea and modulate piglet mucosal immunity and colonic microbiota
Human milk oligosaccharides shorten rotavirus-induced diarrhea and modulate piglet mucosal immunity and colonic microbiota
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DOI：
10.1038/ismej.2014.10
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发表时间：
2014-08-01
期刊：
影响因子：
11
通讯作者：
Donovan, Sharon M.
中科院分区：
文献类型：
--
作者：
Li, Min;Monaco, Marcia H.;Donovan, Sharon M.
在仔猪模型中研究了人乳低聚糖（HMO）对粘膜免疫、肠道菌群和对轮状病毒（RV）感染应答的影响。用单独的配方奶粉（FF）或添加有4 g l（-1）HMO（HMO）或9：1短链低聚半乳糖（3.6 g l（-1））和长链低聚果糖（0.4 g l（-1））的益生元混合物（PRE）的配方奶粉喂养新生仔猪（每组n = 19-21）15天。在第10天用猪轮状病毒（RV）OSU株经口感染每个饮食组中的仔猪（n = 7-8），每天评估粪便稠度。在第15天收集血液、小肠和结肠内容物。检测血清RV特异性抗体浓度、肠道组织形态学、RV非结构蛋白4（NSP 4）和细胞因子mRNA表达。测量结肠内容物pH值、干物质（DM）和短链脂肪酸浓度。通过16 S rRNA基因v1-3区焦磷酸测序分析升结肠微生物群。HMO和PRE饲喂组的腹泻持续时间短于FF仔猪。感染改变肠道组织形态学，增加血清RV特异性抗体反应和肠道RV NSP 4表达，并调制回肠细胞因子的表达。HMO增强了回肠中的T辅助细胞1型（干扰素-γ）和抗炎细胞因子（白细胞介素-10），而益生元促进了RV特异性免疫球蛋白M对感染的反应。RV感染和HMO补充改变了腔内环境和肠道微生物群。HMO增加了pH值和降低DM结肠内容物，并提高了丰富的未分类的毛螺菌科，其中包含许多丁酸生产细菌。总之，HMO和益生元不能预防RV感染的发生，但可以部分通过调节结肠微生物群和对RV感染的免疫反应来减少RV诱导的仔猪腹泻的持续时间。
The impact of human milk oligosaccharides (HMO) on mucosal immunity, gut microbiota and response to rotavirus (RV) infection was investigated in the piglet model. Newborn piglets were fed with formula alone (FF) or formula supplemented with 4 g l(-1) HMO (HMO) or a prebiotic mixture of 9:1 short-chain galactooligosaccharides (3.6 g l(-1)) and long-chain fructooligosaccharides (0.4 g l(-1)) (PRE) (n = 19-21 per group) for 15 days. Piglets (n = 7-8) in each dietary group were orally infected with porcine rotavirus (RV) OSU strain on d10, and stool consistency was assessed daily. Blood, small intestine and colonic contents were collected at day 15. Serum RV-specific antibody concentrations, intestinal histomorphology, RV non-structural protein-4 (NSP4) and cytokine mRNA expression were assessed. Colonic content pH, dry matter (DM) and short-chain fatty acid concentrations were measured. Ascending colonic microbiota was analyzed by 16S rRNA gene v1-3 region pyrosequencing. HMO-and PRE-fed groups had shorter duration of diarrhea than FF piglets. Infection changed intestinal histomorphology, increased serum RV-specific antibody response and intestinal RV NSP4 expression, and modulated ileal cytokine expression. HMO enhanced T helper type 1 (interferon-gamma) and anti-inflammatory (interleukin-10) cytokines in the ileum, while prebiotics promoted RV-specific immunoglobulin M response to the infection. RV infection and HMO supplementation altered intraluminal environment and gut microbiota. HMO increased pH and lowered DM of colonic contents and enhanced the abundance of unclassified Lachnospiraceae, which contains numerous butyrate-producing bacteria. In conclusion, HMO and prebiotics did not prevent the onset of RV infection but reduced the duration of RV-induced diarrhea in piglets, in part, by modulating colonic microbiota and immune response to RV infection.