BackgroundEnterotoxigenic Escherichia coli (ETEC) causes diarrhea in humans, cows, and pigs. The gut microbiota underlies pathology of several infectious diseases yet the role of the gut microbiota in the pathogenesis of ETEC-induced diarrhea is unknown.ResultsBy using an ETEC induced diarrheal model in piglet, we profiled the jejunal and fecal microbiota using metagenomics and 16S rRNA sequencing. A jejunal microbiota transplantation experiment was conducted to determine the role of the gut microbiota in ETEC-induced diarrhea. ETEC-induced diarrhea influenced the structure and function of gut microbiota. Diarrheal piglets had lower Bacteroidetes: Firmicutes ratio and microbiota diversity in the jejunum and feces, and lower percentage of Prevotella in the feces, but higher Lactococcus in the jejunum and higher Escherichia-Shigella in the feces. The transplantation of the jejunal microbiota from diarrheal piglets to uninfected piglets leaded to diarrhea after transplantation. Microbiota transplantation experiments also supported the notion that dysbiosis of gut microbiota is involved in the immune responses in ETEC-induced diarrhea.ConclusionWe conclude that ETEC infection influences the gut microbiota and the dysbiosis of gut microbiota after ETEC infection mediates the immune responses in ETEC infection.Electronic supplementary materialThe online version of this article (10.1186/s12917-018-1704-9) contains supplementary material, which is available to authorized users.

The purpose of this study was to determine the effects of resveratrol (RSV) and the molecular mechanisms by which it regulates vascular smooth muscle contraction and blood pressure in mice. In cultured human vascular smooth muscle cells (VSMCs), we found that the activation of AMP-activated protein kinase (AMPK) by RSV inhibited angiotensin II (AngII)-induced phosphorylation of myosin phosphatase-targeting subunit 1 (MYPT1) and myosin light chain (MLC). Inversely, AMPK inhibition with RNA interference and compound C, an AMPK inhibitor, abolished the inhibitory effect of RSV on AngII-induced MYPT1 and MLC phosphorylation. Thiazovivin, a Rho-associated kinase (ROCK) inhibitor, reversed AngII-induced MYPT1 and MLC phosphorylation, suggesting that ROCK functions as an upstream kinase for MYPT1/MLC. RSV reversed AngII-induced Ras homolog gene family member A (RhoA) and ROCK activity, whereas AMPK inhibition via pharmacological or genetic means abolished this effect. In addition, gene silencing of p190-guanosine triphosphatase-activating protein blocked the effects of RSV-induced AMPK activation on MLC, MYPT1 and RhoA in VSMCs. Ex vivo analyses demonstrated that AngII-induced aorta contractions were dramatically inhibited by RSV, and this effect was abolished by AMPK inhibition. Finally, daily chronic administration of RSVl alleviated hypertension in the experimental model of AngII-induced hypertensive mice, and these effects were accompanied by the activation of AMPK, significantly decreased RhoA activity and phosphorylation levels of MYPT1 and MLC in AngII-treated murine aortic VSMCs. More importantly, administration of compound C significantly abolished the effects of RSV. In conclusion, AMPK suppression of the p190-GAP-dependent RhoA/ROCK/MYPT1/MLC pathway contributes to the hypotensive effect of RSV in AngII-treated mice.

Ferulic acid (FA) and vanillic acid (VA) are considered as major phenolic metabolites of cyanidin 3-glucoside, a polyphenol that widely exists in plants that possess a protective effect against oxidative stress and inflammation in our previous study. This study aimed to investigate the effect of FA and VA on inflammation, gut barrier function, and growth performance in a weaned piglet model challenged with lipopolysaccharide (LPS). Thirty-six piglets (PIC 337 × C48, 28 d of age) were randomly allocated into 3 treatments with 6 replicate pens (2 piglets per pen). They were fed with a basal diet or a diet containing 4,000 mg/kg of FA or VA. Dietary supplementation of VA significantly increased average daily gain (ADG) (P < 0.05). Both FA and VA decreased serum levels of thiobarbituric acid reactive substances (TBARS), interlukin (IL)-1β, IL-2, IL-6, and tumor necrosis factor (TNF)-α ( P < 0.05), and enhanced the expression of tight junction protein oclaudin ( P < 0.05). Analysis of gut microbiota indicated that both FA and VA increased the Firmicutes/Bacteroidetes ratio alongside reducing the relative abundance of the Prevotellaceae family including Prevotella 9 and Prevotella 2 genera, but enriched the Lachoiraceaea family including the Lachnospiraceae FCS020 group ( P < 0.05). Moreover, VA reduced the relative abundance of Prevotella 7 and Prevotella 1 but enriched Lachnospira , Eubacterium eligens group, and Eubacterium xylanophilum group ( P < 0.05), while FA showed a limited effect on these genera. The results demonstrated that both VA and FA could alleviate inflammation and oxidative stress, but only VA has a significant positive effect on the growth performance of LPS-challenged piglets potentially through modulating gut microbiota.

This study aimed to explore the effects of beta-hydroxy-beta-methyl butyrate (HMB) on serum metabolic profiles and meat quality of muscles in Wenshi broiler chickens. Birds were fed a basal diet with an additional 0, 0.05, 0.10, or 0.15% HMB, respectively. Results showed that dietary HMB quadratically increased the average daily gain (P = 0.058) and decreased feed:gain (P &lt; 0.05) mainly in the starter phase. At 51 days of age, birds receiving 0.10% HMB diet exhibited less abdominal fat and more breast yield than the control (P &lt; 0.05). Moreover, dietary HMB quadratically decreased the L∗ value and drip loss in selected muscles (P &lt; 0.05) and increased the a∗ value in breast muscle (P &lt; 0.05). Serum metabolome profiling showed that the most differentially abundant metabolites are lipids and lipid-like molecules, including phosphatidylcholines. It was concluded that HMB improved growth performance and meat quality of muscle in broilers.

Dietary 1% d-Asp and l-Asp affect the growth performance and inflammation in young pigs, which might be associated with gut microbiota.