背景:由a虫和heterapinarum引起的鸡的肠道感染与宿主表现受损有关,特别是在高性能基因型中。鸡异株也是嗜血组织单胞菌的载体,通常与a虫感染有关。这里,我们提供了对鸡血浆和肝脏代谢组的改变的初步见解,作为一个结果的胃肠道线虫感染,并伴有组织瘤。基于1H核磁共振(1H-NMR)的代谢组学与生物信息学分析相结合,用于探索实验感染的鸡(N=108)的肝脏(N=105)和血浆样品的代谢物谱的变化。galli和H.gallinarum(H.meleagridis)。将其与感染后不同周(wpi2、4、6、10、14、18)的未感染鸡进行比较,代表蠕虫的不同发育阶段。
结果:对血浆和肝脏水提取物中的31和54种代谢物进行了定量,分别。统计学分析显示在感染和未感染的母鸡之间的54种鉴定的肝脏代谢物中的任一种中没有显著差异(P>0.05)。相比之下,20种血浆代谢物,包括,氨基酸,糖,糖和有机酸在感染母鸡中的浓度显着升高(P<0.05)。血浆代谢物的变化尤其发生在wpi2、6和10中,涵盖了蠕虫感染的专利期。在这些时间点具有最高变异的血浆代谢物包括谷氨酸,琥珀酸盐,三甲胺-N-氧化物,肌醇,和醋酸盐。差异途径分析表明,感染引起的变化在(1)苯丙氨酸,酪氨酸,和色氨酸代谢,(2)丙氨酸,天冬氨酸和谷氨酸代谢;和3)精氨酸和脯氨酸代谢(路径影响>0.1,FDR调整P值<0.05)。
结论:结论:基于1H-NMR的代谢组学显示,感染肠道病原体A的高性能鸡的血浆代谢组发生了显着变化。Galli和H.Gallinarum.这些改变表明主要在感染通畅期间关键代谢途径的上调。这种方法扩展了我们在代谢水平上对宿主与胃肠道线虫相互作用的理解。
BACKGROUND: Gut infections of chickens caused by Ascaridia galli and Heterakis gallinarum are associated with impaired host performance, particularly in high-performing genotypes. Heterakis gallinarum is also a vector of Histomonas meleagridis that is often co-involved with ascarid infections. Here, we provide a first insight into the alteration of the chicken plasma and liver metabolome as a result of gastrointestinal nematode infections with concomitant histomonosis. 1H nuclear magnetic resonance (1H-NMR) based-metabolomics coupled with a bioinformatics analysis was applied to explore the variation in the metabolite profiles of the liver (N = 105) and plasma samples from chickens (N = 108) experimentally infected with A. galli and H. gallinarum (+H. meleagridis). This was compared with uninfected chickens at different weeks post-infection (wpi 2, 4, 6, 10, 14, 18) representing different developmental stages of the worms.
RESULTS: A total of 31 and 54 metabolites were quantified in plasma and aqueous liver extracts, respectively. Statistical analysis showed no significant differences (P > 0.05) in any of the 54 identified liver metabolites between infected and uninfected hens. In contrast, 20 plasma metabolites including, amino acids, sugars, and organic acids showed significantly elevated concentrations in the infected hens (P < 0.05). Alterations of plasma metabolites occurred particularly in wpi 2, 6 and 10, covering the pre-patent period of worm infections. Plasma metabolites with the highest variation at these time points included glutamate, succinate, trimethylamine-N-oxide, myo-inositol, and acetate. Differential pathway analysis suggested that infection induced changes in (1) phenylalanine, tyrosine, and tryptophan metabolism, (2) alanine, aspartate and glutamate metabolism; and 3) arginine and proline metabolism (Pathway impact > 0.1 with FDR adjusted P-value < 0.05).
CONCLUSIONS: In conclusion, 1H-NMR based-metabolomics revealed significant alterations in the plasma metabolome of high performing chickens infected with gut pathogens-A. galli and H. gallinarum. The alterations suggested upregulation of key metabolic pathways mainly during the patency of infections. This approach extends our understanding of host interactions with gastrointestinal nematodes at the metabolic level.