Bing Yu

Dietary Lactobacillus rhamnosus GG Supplementation Improves the Mucosal Barrier Function in the Intestine of Weaned Piglets Challenged by Porcine Rotavirus

Lactobacillus rhamnosus GG (LGG) has been regarded as a safe probiotic strain. The aim of this study was to investigate whether dietary LGG supplementation could alleviate diarrhea via improving jejunal mucosal barrier function in the weaned piglets challenged by RV, and further analyze the potential roles for apoptosis of jejunal mucosal cells and intestinal microbiota. A total of 24 crossbred barrows weaned at 21 d of age were assigned randomly to 1 of 2 diets: the basal diet and LGG supplementing diet. On day 11, all pigs were orally infused RV or the sterile essential medium. RV infusion increased the diarrhea rate, increased the RV-Ab, NSP4 and IL-2 concentrations and the Bax mRNA levels of jejunal mucosa (P<0.05), decreased the villus height, villus height: crypt depth, the sIgA, IL-4 and mucin 1 concentrations and the ZO-1, occludin and Bcl-2 mRNA levels of jejunal mucosa (P<0.05), and affected the microbiota of ileum and cecum (P<0.05) in the weaned pigs. Dietary LGG supplementation increased the villus height and villus height: crypt depth, the sIgA, IL-4, mucin 1 and mucin 2 concentrations, and the ZO-1, occludin and Bcl-2 mRNA levels of the jejunal mucosa (P<0.05) reduced the Bax mRNA levels of the jejunal mucosa (P<0.05) in weaned pigs. Furthermore, dietary LGG supplementation alleviated the increase of diarrhea rate in the weaned pigs challenged by RV (P<0.05), and relieve the effect of RV infection on the villus height, crypt depth and the villus height: crypt depth of the jejunal mucosa (P<0.05), the NSP4, sIgA, IL-2, IL-4, mucin 1 and mucin 2 concentrations of jejunal mucosa (P<0.05), the ZO-1, occludin, Bax and Bcl-2 mRNA levels of the jejunal mucosa (P<0.05), and the microbiota of ileum and cecum (P<0.05) in the weaned pigs challenged by RV. These results suggest that supplementing LGG in diets alleviated the diarrhea of weaned piglets challenged by RV via inhibiting the virus multiplication and improving the jejunal mucosal barrier function, which was possibly due to the decreasing apoptosis of jejunal mucosal cells and the improvement of intestinal microbiota.

Oxidative stress-induced diseases and tea polyphenols

Reactive oxide species are the middle products of normal metabolism, and play a crucial role in cell signaling transduction. On the contrary, accumulation of excess reactive oxide species results in oxidative stress that often brings multifarious impairment to cells, including decrease of ATP level in cells, elevation of cytosolic Ca2+, DNA damage, dysfunction of biological function in lipid bilayer and so on. These effects will finally lead to all kinds of diseases. Tea polyphenols are widely considered as a kind of excellent antioxidant agents. It can be antioxidants by directly scavenging reactive oxide species or chelating transition metals, and indirectly upregulating the activity of antioxidant enzymes. In addition, tea polyphenols have also been observed a potent pro-oxidant capacity, which directly leads to the generation of reactive oxide species, and indirectly induces apoptosis and death of cancer cells. The underlying characters of its pro-oxidant activity in some diseases is not well understood. The present review we will discuss the dual character of tea polyphenols, both antioxidant and pro-oxidant properties, in some human diseases induced by oxidative stress.

FoxO1: a novel insight into its molecular mechanisms in the regulation of skeletal muscle differentiation and fiber type specification

FoxO1, a member of the forkhead transcription factor forkhead box protein O (FoxO) family, is predominantly expressed in most muscle types. FoxO1 is a key regulator of muscle growth, metabolism, cell proliferation and differentiation. In the past two decades, many researches have indicated that FoxO1 is a negative regulator of skeletal muscle differentiation while contrasting opinions consider that FoxO1 is crucial for myoblast fusion. FoxO1 is expressed much higher in fast twitch fiber enriched muscles than in slow muscles and is also closely related to muscle fiber type specification. In this review, we summarize the molecular mechanisms of FoxO1 in the regulation of skeletal muscle differentiation and fiber type specification.

Dietary Leucine Supplementation Improves the Mucin Production in the Jejunal Mucosa of the Weaned Pigs Challenged by Porcine Rotavirus.

The present study was mainly conducted to determine whether dietary leucine supplementation could attenuate the decrease of the mucin production in the jejunal mucosa of weaned pigs infected by porcine rotavirus (PRV). A total of 24 crossbred barrows weaned at 21 d of age were assigned randomly to 1 of 2 diets supplemented with 1.00% L-leucine or 0.68% L-alanine (isonitrogenous control) for 17 d. On day 11, all pigs were orally infused PRV or the sterile essential medium. During the first 10 d of trial, dietary leucine supplementation could improve the feed efficiency (P = 0.09). The ADG and feed efficiency were impaired by PRV infusion (P<0.05). PRV infusion also increased mean cumulative score of diarrhea, serum rotavirus antibody concentration and crypt depth of the jejunal mucosa (P<0.05), and decreased villus height: crypt depth (P = 0.07), goblet cell numbers (P<0.05), mucin 1 and 2 concentrations (P<0.05) and phosphorylated mTOR level (P<0.05) of the jejunal mucosa in weaned pigs. Dietary leucine supplementation could attenuate the effects of PRV infusion on feed efficiency (P = 0.09) and mean cumulative score of diarrhea (P = 0.09), and improve the effects of PRV infusion on villus height: crypt depth (P = 0.06), goblet cell numbers (P<0.05), mucin 1 (P = 0.08) and 2 (P = 0.07) concentrations and phosphorylated mTOR level (P = 0.08) of the jejunal mucosa in weaned pigs. These results suggest that dietary 1% leucine supplementation alleviated the decrease of mucin production and goblet cell numbers in the jejunal mucosa of weaned pigs challenged by PRV possibly via activation of the mTOR signaling.

Chronic glucocorticoid exposure-induced epididymal adiposity is associated with mitochondrial dysfunction in white adipose tissue of male C57BL/6J mice.

Prolonged and excessive glucocorticoids (GC) exposure resulted from Cushings syndrome or GC therapy develops central obesity. Moreover, mitochondria are crucial in adipose energy homeostasis. Thus, we tested the hypothesis that mitochondrial dysfunction may contribute to chronic GC exposure-induced epididymal adiposity in the present study. A total of thirty-six 5-week-old male C57BL/6J mice (∼20 g) were administrated with 100 µg/ml corticosterone (CORT) or vehicle through drinking water for 4 weeks. Chronic CORT exposure mildly decreased body weight without altering food and water intake in mice. The epididymal fat accumulation was increased, but adipocyte size was decreased by CORT. CORT also increased plasma CORT, insulin, leptin, and fibroblast growth factor 21 concentrations as measured by RIA or ELISA. Interestingly, CORT increased plasma levels of triacylglycerols and nonesterified fatty acids, and up-regulated the expression of both lipolytic and lipogenic genes as determined by real-time RT-PCR. Furthermore, CORT impaired mitochondrial biogenesis and oxidative function in epididymal WAT. The reactive oxygen species production was increased and the activities of anti-oxidative enzymes were reduced by CORT treatment as well. Taken together, these findings reveal that chronic CORT administration-induced epididymal adiposity is, at least in part, associated with mitochondrial dysfunction in mouse epididymal white adipose tissue.

Intestinal microbiota could transfer host Gut characteristics from pigs to mice

BackgroundThe present study was conducted to compare the differences in gut microbiota composition and gut-phenotypes among pig breeds, and determine whether these differences would transmit to mice colonized with fecal microbiota of different pig breeds. A total of 24 1-day-old germ-free BALB/C mice were divided into 3 groups (TFM, YFM and RFM), which were transplanted with intact fecal microbiota of Tibetan pig (TP), Yorkshire pig (YP) and Rongchang pig (RP), respectively.ResultsResults showed that different pig breeds exhibited distinct gut microbiota profile based on high-throughput pyrosequencing. YP exhibited a lower Firmicutes/Bacteroidetes ratio and apparent genera differences compared with RP and TP, and higher levels of bacteria from Spirochaetes were observed in TP compared with RP and YP (P < 0.05). Transplanted porcine microbiota into GF mice replicated the phenotypes of pig donors. Moreover, the three groups of donor pigs and their mice recipients exhibited different intestinal index and morphology. TP and RP had higher intestinal weight and relative CDX2 mRNA expression in ileum than YP, and longer intestine, higher villus height of duodenum and jejunum were observed in TP compared with YP and RP (P < 0.05). TP exhibited higher GLP-2 mRNA expression in duodenum and jejunum than RP (P < 0.05). Similarly, YFM had lower intestine weight and CDX2 mRNA expression in ileum than TFM and RFM (P < 0.05). The intestine length in TFM was longer than that in RFM, and TFM had higher villus height in duodenum and jejunum and GLP-2 mRNA expression in ileum than the other two groups (P < 0.05). Besides, the digestive and absorptive ability was different among the three groups in donor pigs and mice recipients. YP had higher jejunal lactase and maltase activities than TP and RP, while TP had higher activities of jejunal ATPase, γ-GT, and relative SGLT1 mRNA expression in duodenum and jejunum than YP and RP (P < 0.05). Likewise, YFM had higher jejunal sucrase and maltase activities than TFM and RFM, whereas higher jejunal γ-GT activity and relative SGLT1 mRNA expression in duodenum and ileum were observed in TFM compared with YFM and RFM (P < 0.05). In addition, Tibetan pigs-derived microbiota improved gut barrier in mice recipients. The concentration of MDA in YP was higher than that in TP and RP (P = 0.078), and the relative ZO-1 mRNA expression in ileum in TP was higher than that in YP (P < 0.05). Likely, compared with TFM and RFM, YFM exhibited increasing MDA concentration in jejunum (P = 0.098), and the relative ZO-1 mRNA expression in duodenum and ileum in TFM were higher than that in YFM (P < 0.05).ConclusionsThere were huge differences in gut microbiota composition and gut characteristics among pig breeds, and gut microbiota could partially convey host gut characteristics from pigs to mice.

Effect of 25-hydroxyvitamin D3 on rotavirus replication and gene expressions of RIG-I signalling molecule in porcine rotavirus-infected IPEC-J2 cells.

The study evaluated whether a 25-hydroxyvitamin D3 (25D3) supplementation decreases the replication of rotavirus by the retinoic acid-inducible gene I (RIG-I) signalling pathway in a porcine small intestinal epithelial cell line (IPEC-J2). The results show that IPEC-J2 cells express high baseline levels of 1α-hydroxylase (CYP27B1), which converts inactive 25D3 to the active 1,25-dihydroxyvitamin D3 (1,25D3). Porcine rotavirus (PRV) infection alone resulted in a significant increase in CYP27B1 mRNA, which augmented the production of active vitamin D. Physiological concentrations of 25D3 were found to decrease PRV replication in IPEC-J2 cells. RIG-I plays an important role in the recognition of double-stranded RNA virus by host cells. Upon recognition, RIG-I triggers a series of signalling molecules such as interferon-β (IFN-β) promoter stimulator 1 (IPS-1) leading to the expression of type I interferons (IFN-β). Active 25D3 that was generated by PRV-infected IPEC-J2 cells led to an increased expression of toll-like receptors 3 (TLR3), RIG-I, IPS-1, IFN-β and IFN-stimulated genes 15 (ISG15) with important innate immune functions. Inhibiting CYP27B1 also failed to increase RIG-I, IPS-1, IFN-β and ISG15 mRNA expression. These observations suggest that 25D3 can directly inhibit PRV in IPEC-J2 cells, which requires this active form of vitamin D. The anti-rotavirus effect of 25D3 is mediated at least in part by RIG-I signalling pathways in IPEC-J2 cells.

Dietary apple pectic oligosaccharide improves gut barrier function of rotavirus-challenged weaned pigs by increasing antioxidant capacity of enterocytes

Rotavirus can lead to decreasing gut barrier function and diarrhea of children and young animals. Apple pectic oligosaccharide treatment reduced diarrhea in rotavirus-infected piglets. This study was conducted to explore whether apple pectic oligosaccharide administration could protect gut barrier function of piglets against rotavirus infection. A total of 28 crossbred weaned barrows were allotted into 2 treatments fed the diets supplementing 0 and 200 mg/kg apple pectic oligosaccharide. Half of pigs in each diet treatment were challenged by rotavirus on d 15. The whole duration of this experiment is 18 days. Rotavirus challenge increased average diarrhea index, and impaired microbiota in cecal digesta, and histology, expressions of tight-junction proteins, mucins and glucagon like peptide-2 concentrations, antioxidant capacity, endoplasmic reticulum stress, autophagy and apoptosis in jejunal mucosa of piglets. However, dietary apple pectic oligosaccharide supplementation relieved effects of rotavirus challenge on diarrhea, gut health, and antioxidant capacity, endoplasmic reticulum stress, autophagy and apoptosis of jejunal mucosa in piglets. These results suggest that apple pectic oligosaccharide administration can prevent diarrhea and damage of gut barrier function via improving antioxidant capacity that might reduce endoplasmic reticulum stress, autophagy and apoptosis of intestinal epithelial cells in rotavirus-infected piglets.

Modulation of intestine development by fecal microbiota transplantation in suckling pigs

The present study was conducted to investigate the effects of early fecal microbiota transplantation on gut development in sucking piglets. A total of 24 3 day-old DLY sucking piglets (2.11 ± 0.15) kg were randomly divided into four groups (TMP, YMP, RMP and control group (CON)), which were transplanted with intact fecal microbiota of Tibetan pig (TP), Yorkshire pig (YP), Rongchang pig (RP), and without transplantation, respectively. The whole trial lasted for 56 d. The results are as follows: when compared with the YMP and RMP treatments, TMP and CON had a lower diarrhea index (P < 0.05), TMP and CON had higher GLP-2 and ANG4 mRNA abundances in the ileum (P < 0.05), and the TMP had a higher jejunal villus height: crypt depth and a higher colonic GLP-2 mRNA abundance (P < 0.05). Moreover, when compared with the YMP and RMP treatments, TMP had an enhanced DMT1 mRNA abundance in the duodenum (P < 0.05), TMP and CON had a greater lactase activity and a higher DMT1 mRNA abundance in the jejunum (P < 0.05), and CON had a higher γ-GT activity in the jejunum (P < 0.05). The jejunal Ca2+, Mg2+-ATPase activity in TMP was higher than that in CON, and the jejunal Na+, K+-ATPase activity in TMP was higher than that in the other three treatments (P < 0.05). Besides, when compared with the YMP and RMP treatments, TMP had a lower MDA content and a higher MUC1 mRNA abundance in the jejunum (P < 0.05); CON had a higher SOD activity in the jejunum (P < 0.05), whereas TMP and CON had a higher butyric acid concentration in the colon and a lower LPS content in the serum (P < 0.05). Finally, when compared with the TMP treatment, the other three treatments had an enhanced IL-10 mRNA abundance in the colon (P < 0.05), YMP and CON had higher counts of Escherichia coli in the colonic digesta (P < 0.05), and the CON had lower counts of Lactobacillus spp in the cecal and colonic digesta (P < 0.05). These data indicated that early transplantation of the fecal microbiota from the Yorkshire pigs and Rongchang pigs to DLY suckling piglets would destroy the gut microbiota balance and thus damage intestinal health.

Fungi in Gastrointestinal Tracts of Human and Mice: from Community to Functions

Fungi are often ignored in studies on gut microbes because of their low level of presence (making up only 0.1% of the total microorganisms) in the gastrointestinal tract (GIT) of monogastric animals. Recent studies using novel technologies such as next generation sequencing have expanded our understanding on the importance of intestinal fungi in humans and animals. Here, we provide a comprehensive review on the fungal community, the so-called mycobiome, and their functions from recent studies in humans and mice. In the GIT of humans, fungi belonging to the phyla Ascomycota, Basidiomycota and Chytridiomycota are predominant. The murine intestines harbor a more diverse assemblage of fungi. Diet is one of the major factors influencing colonization of fungi in the GIT. Presence of the genus Candida is positively associated with dietary carbohydrates, but are negatively correlated with dietary amino acids, proteins, and fatty acids. However, the relationship between diet and the fungal community (and functions), as well as the underlying mechanisms remains unclear. Dysbiosis of intestinal fungi can cause invasive infections and inflammatory bowel diseases (IBD). However, it is not clear whether dysbiosis of the mycobiome is a cause, or a result of IBD. Compared to non-inflamed intestinal mucosa, the abundance and diversity of fungi is significantly increased in the inflamed mucosa. The commonly observed commensal fungal species Candida albicans might contribute to occurrence and development of IBD. Limited studies show that Candida albicans might interact with immune cells of the host intestines through the pathways associated with Dectin-1, Toll-like receptor 2 (TLR2), and TLR4. This review is expected to provide new thoughts for future studies on intestinal fungi and for new therapies to fungal infections in the GIT of human and animals.