Effects of dechlorane plus on intestinal barrier function and intestinal microbiota of Cyprinus carpio L

2020 ◽  
Vol 204 ◽  
pp. 111124
Author(s):  
Baohua Li ◽  
Jianjun Chen ◽  
Songyun Wang ◽  
Pengju Qi ◽  
Xulu Chang ◽  
...  
Keyword(s):  
Intestinal Microbiota ◽  
Cyprinus Carpio ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Dechlorane Plus

scholarly journals Intake of a Mixture of Sake Cake and Rice Malt Increases Mucin Levels and Changes in Intestinal Microbiota in Mice

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 449 ◽  
Author(s):  
Shinpei Kawakami ◽  
Ryouichi Ito ◽  
Hiroko Maruki-Uchida ◽  
Asuka Kamei ◽  
Akihito Yasuoka ◽  
...  
Keyword(s):  
Gene Expression ◽  
Intestinal Microbiota ◽  
Barrier Function ◽  
Gene Expression Analysis ◽  
Control Diet ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
The Family ◽  
Family Level ◽  
Muc2 Expression

Amazake is a traditional Japanese beverage. Its main ingredients are sake cake and rice malt. In this study, we examined the effect of sake cake and rice malt on the intestinal barrier function and gut microbiota. BALB/c mice were fed a control diet or a diet containing a mixture of sake cake and rice malt powder (SRP) for four weeks. Fecal IgA values did not change between groups, but the fecal mucin level was significantly greater in the SRP-fed group. Gene expression analysis in the ileum by real-time PCR demonstrated Muc2 expression did not change, while the Muc3 expression was upregulated in the SRP-fed group. Furthermore, microbiota analysis demonstrated a change by SRP intake at the family level, and the proportion of Lactobacillaceae significantly increased in the SRP-fed group. At the genus level, the proportion of Lactobacillus also significantly increased in the SRP-fed group. These results suggest that the intake of a mixture of sake cake and rice malt improves intestinal barrier function by increasing mucin levels and inducing changes in intestinal microbiota.

scholarly journals Bile acid supplementation improves murine pancreatitis in association with the gut microbiota

2020 ◽  
Author(s):  
You-Dong Wan ◽  
Rui-Xue Zhu ◽  
Xin-Ting Pan
Keyword(s):  
Bile Acid ◽  
Gut Microbiota ◽  
Intestinal Microbiota ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Pancreatic Injury ◽  
Farnesoid X Receptor ◽  
Intestinal Barrier Function ◽  
Signaling Receptors

ABSTRACTDisorders of bile acids (BAs) are closely related to the development of liver and intestinal diseases, including acute pancreatitis (AP). However, the mechanism underlying the involvement of BAs in AP development remains unclear. We used intraperitoneal injection of cerulein to construct AP mouse models. These mice had significantly reduced tauroursodeoxycholic acid (TUDCA) and an imbalance of intestinal microbiota, based on 16S rDNA gene sequencing. To explore the role of AP-induced intestinal microbiota changes in the development of AP, we transplanted stool obtained from AP mice to antibiotic-treated, microbiota-depleted healthy mice. Microbiota-depleted mice presented injury to the intestinal barrier function and pancreas. Additionally, microbiota depletion reduced AP-associated pancreatic injury. This indicated that the gut microbiota may worsen AP. As TUDCA was deficient in AP mice, we gavaged AP mice with it, and evaluated subsequent expression changes in the bile acid signaling receptors farnesoid-x-receptor (FXR) and its target gene fibroblast growth factor (FGF) 15. These were downregulated, and pancreatic and intestinal barrier function injury were mitigated. Similar results were found in microbiota-depleted AP without BA treatment. However, we did not observe further downregulation of the FXR signaling pathway in microbiota-depleted AP mice given TUDCA, indicating that improvement of pancreatitis by TUDCA may be associated with gut microbiota. Our analysis of changes to the gut microbiota in AP indicated that Lactobacilli may be the key contributors. Taken together, our study shows that supplementation with BAs could improve bile acid-FXR-FGF15 signaling, and reduce pancreatic and intestinal injury, and that this effect may be associated with the gut microbiota.

scholarly journals Anethole Attenuates Enterotoxigenic Escherichia coli-Induced Intestinal Barrier Disruption and Intestinal Inflammation via Modification of TLR Signaling and Intestinal Microbiota

2021 ◽  
Vol 12 ◽  
Author(s):  
Qingyuan Yi ◽  
Jiaxin Liu ◽  
Yufeng Zhang ◽  
Hanzhen Qiao ◽  
Fang Chen ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Growth Performance ◽  
Mrna Expression ◽  
Intestinal Microbiota ◽  
Barrier Function ◽  
Intestinal Inflammation ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Weaned Piglets ◽  
Tnf Α

This study aimed to investigate the effects of dietary anethole supplementation on the growth performance, intestinal barrier function, inflammatory response, and intestinal microbiota of piglets challenged with enterotoxigenic Escherichia coli K88. Thirty-six weaned piglets (24 ± 1 days old) were randomly allocated into four treatment groups: (1) sham challenge (CON); (2) Escherichia coli K88 challenge (ETEC); (3) Escherichia coli K88 challenge + antibiotics (ATB); and (4) Escherichia coli K88 challenge + anethole (AN). On day 12, the piglets in the ETEC, ATB, and AN group were challenged with 10 mL E. coli K88 (5 × 109 CFU/mL), whereas the piglets in the CON group were orally injected with 10 mL nutrient broth. On day 19, all the piglets were euthanized for sample collection. The results showed that the feed conversion ratio (FCR) was increased in the Escherichia coli K88-challenged piglets, which was reversed by the administration of antibiotics or anethole (P < 0.05). The duodenum and jejunum of the piglets in ETEC group exhibited greater villous atrophy and intestinal morphology disruption than those of the piglets in CON, ATB, and AN groups (P < 0.05). Administration of anethole protected intestinal barrier function and upregulated mucosal layer (mRNA expression of mucin-1 in the jejunum) and tight junction proteins (protein abundance of ZO-1 and Claudin-1 in the ileum) of the piglets challenged with Escherichia coli K88 (P < 0.05). In addition, administration of antibiotics or anethole numerically reduced the plasma concentrations of IL-1β and TNF-α (P < 0.1) and decreased the mRNA expression of TLR5, TLR9, MyD88, IL-1β, TNF-α, IL-6, and IL-10 in the jejunum of the piglets after challenge with Escherichia coli K88 (P < 0.05). Dietary anethole supplementation enriched the abundance of beneficial flora in the intestines of the piglets. In summary, anethole can improve the growth performance of weaned piglets infected by ETEC through attenuating intestinal barrier disruption and intestinal inflammation.

scholarly journals Effect of Dietary Clostridium butyricum Supplementation on Growth Performance, Intestinal Barrier Function, Immune Function, and Microbiota Diversity of Pekin Ducks

Animals ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 2514
Author(s):  
Yanhan Liu ◽  
Cun Liu ◽  
Keying An ◽  
Xiaowei Gong ◽  
Zhaofei Xia
Keyword(s):  
Growth Performance ◽  
Mrna Expression ◽  
Intestinal Microbiota ◽  
Relative Abundance ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Expression Levels ◽  
Pekin Ducks ◽  
Mrna Expression Levels

Clostridium butyricum (C. butyricum) is increasingly being used to test the promotion of the gut health of animals. However, the modes of action for such applications for waterfowl remain unclear. Thus, we investigated whether or not intestinal barrier function, immune-related gene expression, and the diversity of the intestinal microbiota in Pekin ducks varied under C. butyricum supplementation. A total of 500 ducks were randomly assigned into five treatments supplemented with basal diets containing: either 0 (group Control), 200 (group CB200), 400 (group CB400) and 600 (group CB600) mg/kg C. butyricum or 150 mg/kg aureomycin (group A150) for 42 days. In comparison with the control group, C. butyricum supplementation enhanced the growth performance and intestinal villus height of Pekin ducks at 42 d. Serum immune indexes and fecal short-chain fatty acids (SCFAs) were all improved at both 21 d and 42 d after C. butyricum addition. The mRNA expression levels of Mucin2, Zonula occludens-1 (ZO-1), Caudin-3, and Occludin increased at 21 d and 42 d and the mRNA expression levels of IL-4 and IL-10 only increased at 42 d after C. butyricum addition. Dietary C. butyricum also resulted in an increase in the number of diversities of operational taxonomic units (OTUs), and an increase in the α-diversity of intestinal microbiota. The addition of C. butyricum altered the composition of the intestinal microbiota from 21 d to 42 d. The relative abundance of Firmicutes and Bacteroidetes showed little changes among groups; however, the relative abundance of Firmicutes/Bacteroidetes were found to have been significantly different between the 21 d and 42 d. C. butyricum administration improved the intestinal health of Pekin ducks by increasing the diversity of intestinal microbiota, enhancing the SCFAs contents, and strengthening the intestinal barrier function and immune systems. The optimal dietary supplementation dosage was recommended as 400 mg/kg in the diet.

scholarly journals Effects of Tylosin on Bacterial Mucolysis, Clostridium perfringens Colonization, and Intestinal Barrier Function in a Chick Model of Necrotic Enteritis

2003 ◽  
Vol 47 (10) ◽  
pp. 3311-3317 ◽  
Author(s):  
C. T. Collier ◽  
J. D. van der Klis ◽  
B. Deplancke ◽  
D. B. Anderson ◽  
H. R. Gaskins
Keyword(s):  
Clostridium Perfringens ◽  
Intestinal Microbiota ◽  
Barrier Function ◽  
Disease Risk ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Current Debate ◽  
Rrna Gene ◽  
Necrotic Enteritis ◽  
The Impact

ABSTRACT Necrotic enteritis (NE) is a worldwide poultry disease caused by the alpha toxin-producing bacterium Clostridium perfringens. Disease risk factors include concurrent coccidial infection and the dietary use of cereal grains high in nonstarch polysaccharides (NSP), such as wheat, barley, rye, and oats. Outbreaks of NE can be prevented or treated by the use of in-feed antibiotics. However, the current debate regarding the prophylactic use of antibiotics in animal diets necessitates a better understanding of factors that influence intestinal colonization by C. perfringens as well as the pathophysiological consequences of its growth. We report a study with a chick model of NE, which used molecular (16S rRNA gene [16S rDNA]) and culture-based microbiological techniques to investigate the impact of the macrolide antibiotic tylosin phosphate (100 ppm) and a dietary NSP (pectin) on the community structure of the small intestinal microbiota relative to colonization by C. perfringens. The effects of tylosin and pectin on mucolytic activity of the microbiota and C. perfringens colonization and their relationship to pathological indices of NE were of particular interest. The data demonstrate that tylosin reduced the percentage of mucolytic bacteria in general and the concentration of C. perfringens in particular, and these responses correlated in a temporal fashion with a reduction in the occurrence of NE lesions and an improvement in barrier function. The presence of pectin did not significantly affect the variables measured. Thus, it appears that tylosin can control NE through its modulation of C. perfringens colonization and the mucolytic activity of the intestinal microbiota.

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