scholarly journals Emodin Improves Intestinal Health and Immunity through Modulation of Gut Microbiota in Mice Infected by Pathogenic Escherichia coli O1

Animals ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 3314
Author(s):  
Ruijuan Gao ◽  
Chunjie Wang ◽  
Aricha Han ◽  
Yanping Tian ◽  
Shunan Ren ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Intestinal Microbiota ◽  
Goblet Cells ◽  
Mucosal Barrier ◽  
Intestinal Damage ◽  
Mrna Levels ◽  
Rt Pcr ◽  
Intestinal Mucosal Barrier ◽  
E Coli ◽  
Mucosal Barrier Function

The effect of emodin on the intestinal mucosal barrier of a mouse E. coli O1-induced diarrhea model was observed. Following successful establishment of a diarrhea model, the mice were treated with drugs for seven days. Intestinal lesions and the shape and the number of goblet cells were assessed via hematoxylin-eosin and periodic-acid-Schiff staining, while changes in inflammatory factors, ultrastructure of the small intestine, expression of MUC-2, and changes in the intestinal microbiota were analyzed via RT-PCR, electron microscopy, immunofluorescence, and 16S rRNA sequencing. Examination showed that emodin ameliorated pathological damage to the intestines of diarrheic mice. RT-PCR indicated that emodin reduced TNF-α, IL-β, IL-6, MPO, and COX-2 mRNA levels in duodenal tissues and increased the levels of sIgA and MUC-2 and the number of goblet cells. Microbiome analysis revealed that Escherichia coli O1 reduced bacterial richness and altered the distribution pattern of bacterial communities at the phylum and order levels in cecum contents. Notably, pathogenic Clostridiales and Enterobacteriales were significantly increased in diarrheic mice. However, emodin reversed the trend. Thus, emodin protected against intestinal damage induced by E. coli O1 and improved intestinal mucosal barrier function in mice by increasing the abundance of beneficial intestinal microbiota and inhibiting the abundance of harmful bacteria, thereby alleviating diarrhea.

scholarly journals Dietary l-Tryptophan Supplementation Enhances the Intestinal Mucosal Barrier Function in Weaned Piglets: Implication of Tryptophan-Metabolizing Microbiota

2018 ◽  
Vol 20 (1) ◽  
pp. 20 ◽  
Author(s):  
Haiwei Liang ◽  
Zhaolai Dai ◽  
Jiao Kou ◽  
Kaiji Sun ◽  
Jingqing Chen ◽  
...  
Keyword(s):  
Tight Junction ◽  
Mucosal Barrier ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Tight Junction Proteins ◽  
Weaned Piglets ◽  
Intestinal Mucosal Barrier ◽  
Mucosal Barrier Function ◽  
Small Intestinal ◽  
Junction Proteins

l-Tryptophan (Trp) is known to play an important role in the health of the large intestine. However, a role of dietary Trp in the small-intestinal mucosal barrier and microbiota remains poorly understood. The present study was conducted with weaned piglets to address this issue. Postweaning piglets were fed for 4 weeks a corn- and soybean meal-based diet supplemented with 0 (Control), 0.1, 0.2, or 0.4% Trp. The small-intestinal microbiota and serum amino acids were analyzed by bacterial 16S rRNA gene-based high-throughput sequencing methods and high-performance liquid chromatography, respectively. The mRNA levels for genes involved in host defense and the abundances of tight-junction proteins in jejunum and duodenum were measured by real time-PCR and Western blot techniques, respectively. The concentrations of Trp in the serum of Trp-supplemented piglets increased in a dose-dependent manner. Compared with the control group, dietary supplementation with 0.2–0.4% Trp reduced the abundances of Clostridium sensu stricto and Streptococcus in the jejunum, increased the abundances of Lactobacillus and Clostridium XI (two species of bacteria that can metabolize Trp) in the jejunum, and augmented the concentrations of secretory immunoglobulin A (sIgA) as well as mRNA levels for porcine β-defensins 2 and 3 in jejunal tissues. Moreover, dietary Trp supplementation activated the mammalian target of rapamycin signaling and increased the abundances of tight-junction proteins (zonula occludens (ZO)-1, ZO-3, and claudin-1) in jejunum and duodenum. We suggested that Trp-metabolizing bacteria in the small intestine of weaned pigs primarily mediated the beneficial effects of dietary Trp on its mucosal integrity, health, and function.

scholarly journals Multiple Roles for the sRNA GcvB in the Regulation of Slp Levels in Escherichia coli

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Lorraine T. Stauffer ◽  
George V. Stauffer
Keyword(s):  
Escherichia Coli ◽  
Luria Bertani ◽  
Multiple Roles ◽  
Activation Mechanism ◽  
Mrna Levels ◽  
Rt Pcr ◽  
E Coli ◽  
Luria Bertani Broth ◽  
Outer Membrane Lipoprotein ◽  
Membrane Lipoprotein

The Escherichia coli gcvB gene encodes a small RNA that regulates many genes involved in the transport of dipeptides, oligopeptides, and amino acids (oppA, dppA, cycA, and sstT). A microarray analysis of RNA isolated from an E. coli wild-type and a ΔgcvB strain grown to midlog phase in Luria-Bertani broth indicated that genes not involved in transport are also regulated by GcvB. One gene identified was slp that encodes an outer membrane lipoprotein of unknown function induced when cells enter stationary phase. The aim of this study was to verify that slp is a new target for GcvB-mediated regulation. In this study we used RT-PCR to show that GcvB regulates slp mRNA levels. GcvB negatively controls slp::lacZ in cells grown in Luria-Bertani broth by preventing an Hfq-mediated activation mechanism for slp::lacZ expression. In contrast, in glucose minimal medium supplemented with glycine, GcvB is required for inhibition of slp::lacZ expression, and Hfq prevents GcvB-mediated repression. Thus, GcvB regulates slp in both LB and in glucose minimal + glycine media and likely by mechanisms different than how it regulates sstT, dppA, cycA, and oppA. Repression of slp by GcvB results in an increase in resistance to chloramphenicol, and overexpression of slp in a ΔgcvB strain results in an increase in sensitivity to chloramphenicol.

scholarly journals Dietary fibre affects intestinal mucosal barrier function and regulates intestinal bacteria in weaning piglets

2013 ◽  
Vol 110 (10) ◽  
pp. 1837-1848 ◽  
Author(s):  
Hong Chen ◽  
Xiangbing Mao ◽  
Jun He ◽  
Bing Yu ◽  
Zhiqing Huang ◽  
...  
Keyword(s):  
Barrier Function ◽  
Transforming Growth Factor ◽  
Control Diet ◽  
Mucosal Barrier ◽  
Intestinal Barrier Function ◽  
Mrna Levels ◽  
Intestinal Mucosal Barrier ◽  
Junction Protein ◽  
Mucosal Barrier Function ◽  
Weaning Piglets

The objective of the present study was to evaluate the effects of fibre source on intestinal mucosal barrier function in weaning piglets. A total of 125 piglets were randomly allotted on the basis of their body weight and litters to one of five experimental diets, i.e. a control diet without fibre source (CT), and diets in which expanded maize was replaced by 10 % maize fibre (MF), 10 % soyabean fibre (SF), 10 % wheat bran fibre (WBF) or 10 % pea fibre (PF). The diets and water were fed ad libitum for 30 d. Piglets on the WBF and PF diets had lower diarrhoea incidence compared with the MF- and SF-fed animals. A higher ratio of villous height:crypt depth in the ileum of WBF-fed piglets and higher colonic goblet cells in WBF- and PF-fed piglets were observed compared with CT-, MF- and SF-fed piglets. In the intestinal digesta, feeding WBF and PF resulted in increased Lactobacillus counts in the ileum and Bifidobacterium counts in the colon. Lower Escherichia coli counts occurred in the ileum and colon of WBF-fed piglets than in SF-fed piglets. Tight junction protein (zonula occludens 1; ZO-1) and Toll-like receptor 2 (TLR2) gene mRNA levels were up-regulated in the ileum and colon of pigs fed WBF; however, feeding MF and SF raised IL-1α and TNF-α mRNA levels. Furthermore, higher diamine oxidase activities, transforming growth factor-α, trefoil factor family and MHC-II concentration occurred when feeding WBF and PF. In conclusion, the various fibre sources had different effects on the ileal and colonic barrier function. Clearly, WBF and PF improved the intestinal barrier function, probably mediated by changes in microbiota composition and concomitant changes in TLR2 gene expression.

scholarly journals Enhancement of Shiga Toxin Production in Enterohemorrhagic Escherichia coli Serotype O157:H7 by DNase Colicins

2007 ◽  
Vol 73 (23) ◽  
pp. 7582-7588 ◽  
Author(s):  
Hirono Toshima ◽  
Ayana Yoshimura ◽  
Kentaro Arikawa ◽  
Ayumi Hidaka ◽  
Jun Ogasawara ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Clinical Manifestations ◽  
Fold Increase ◽  
Toxin Production ◽  
Enterohemorrhagic Escherichia Coli ◽  
Mrna Levels ◽  
Rt Pcr ◽  
E Coli ◽  
Reverse Transcription Pcr

ABSTRACT Colicins are proteins produced by and active against several strains of Escherichia coli. Previously we reported that colicinogenic bacteria seemed beneficial in preventing the clinical manifestations of infectious disease caused by enterohemorrhagic E. coli O157 in humans. The inhibitory effects could be due to a decrease in O157 levels and/or pathogenicity. This study investigated the effects of colicinogenic E. coli on the production of Shiga toxin (Stx) by O157. Standard strains of colicinogenic bacteria carrying plasmids for each type of colicin (E3/5/8/9) were used for the study. The O157 strains were cultured in the presence of colicinogenic bacteria or extracted colicins. Compared with results for controls, DNase colicins (E8/9) facilitated an 8- to 64-fold increase in production of Stx2, while RNase colicins (E3/5) suppressed Stx production in only two strains. Stx prophages were induced in synchrony with Stx production. Semiquantitative real-time reverse transcription-PCR (RT-PCR) was then performed to examine SOS gene expression. The RT-PCR results clearly indicated a marked increase in mRNA levels of SOS reaction-associated genes after the addition of DNase colicins. We believe that Stx prophages are induced by the SOS response to DNA damage caused by DNase colicins, thus leading to higher Stx production. These findings suggest that while colicinogenic bacteria can be antagonistic to O157 infection, DNase colicins may enhance Stx production. Thus, colicinogenic flora is likely to be involved in the complex pathogenic pathways of O157 infection, and further investigation should be performed before the use of colicinogenic bacteria as an intervention method.

scholarly journals Jinhong Tablet Reduces Damage of Intestinal Mucosal Barrier in Rats with Acute Biliary Infection via Bcl-2/Bax mRNA and Protein Regulation

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Xiaoqiang Liang ◽  
Xiao Ni ◽  
YongQi Wang ◽  
Jinkun Xie ◽  
Xuelin Zhang ◽  
...  
Keyword(s):  
Morphological Changes ◽  
Male Rats ◽  
Mucosal Barrier ◽  
Sham Operation ◽  
Intestinal Damage ◽  
Intestinal Epithelial ◽  
Protein Regulation ◽  
Intestinal Mucosal Barrier ◽  
Biliary Infection ◽  
Mucosal Barrier Function

Objective. To explore the effects and mechanism of Jinhong Tablet on intestinal mucosal barrier function and SIRS in rats with acute biliary infection.Methods. 36 SD male rats were divided into three groups: sham operation (control), acute biliary infection (ABI) model, and Jinhong Tablet (Jinhong) group. Jinhong group were force-fed with Jinhong Tablet, while the other two groups received oral saline. At days 3 and 5, morphological changes of intestinal mucosa were assessed. Serum diamine oxidase (DAO), D-lactate, and endotoxin levels were measured. And the genes bcl-2 and bax in intestinal tissues were tested by real-time PCR and Western blotting.Results. Intestinal damage was significantly less severe in Jinhong group compared with ABI group, as indicated by Chiu’s scoring, TUNEL analysis, and serum DAO, D-lactic acid, and endotoxin levels. Additionally, the expression of bax mRNA and protein was decreased and the ratio of bcl-2/bax mRNA and protein was increased compared with ABI group.Conclusion. Jinhong Tablet had a positive intervention on acute biliary infection through improving inflammation and intestinal mucosal barrier, inhibiting excessive apoptosis of intestinal epithelial cells via bax and bcl-2 gene, and protein regulation.

Sulfation modification enhances the intestinal regulation of Cyclocarya paliurus polysaccharides in cyclophosphamide-treated mice via restoring intestinal mucosal barrier function and modulating gut microbiota

2021 ◽  
Author(s):  
Yue Yu ◽  
Haibin Zhu ◽  
Mingyue Shen ◽  
Qiang Yu ◽  
Yi Chen ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Intestinal Microbiota ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Mucosal Barrier ◽  
Intestinal Mucosal Barrier ◽  
Cyclocarya Paliurus ◽  
Mucosal Barrier Function ◽  
Sulfated Derivative

This work aimed to investigate the effects of a sulfated derivative of Cyclocarya paliurus polysaccharide (SCP3) on cyclophosphamide (CTX)-induced intestinal barrier damage and intestinal microbiota in mice.

Protective effect of dexmedetomidine on intestinal mucosal barrier function in rats after cardiopulmonary bypass

2021 ◽  
pp. 153537022110625
Author(s):  
Tong Jia ◽  
Zhen Xing ◽  
Huijuan Wang and ◽  
Guoli Li
Keyword(s):  
Cardiopulmonary Bypass ◽  
Inflammatory Response ◽  
Barrier Function ◽  
Mucosal Damage ◽  
Mucosal Barrier ◽  
Inflammatory Factors ◽  
Intestinal Damage ◽  
Intestinal Mucosal Barrier ◽  
Mucosal Barrier Function ◽  
Anti Inflammatory

Cardiopulmonary bypass can result in damage to the intestines, leading to the occurrence of systemic inflammatory response syndrome. Dexmedetomidine is reported to confer anti-inflammatory properties. Here, the purpose of this study is to investigate the effect of dexmedetomidine on the intestinal mucosa barrier damage in a rat model of cardiopulmonary bypass. It was observed that cardiopulmonary bypass greatly decreased the levels of hemodynamic parameters than SHAM group, whereas dexmedetomidine pretreatment in a cardiopulmonary bypass model rat prevented this reduction. Also, it showed that compared with control animals, cardiopulmonary bypass caused obvious mucosal damage, which was attenuated in dexmedetomidine + cardiopulmonary bypass group. The above findings were in line with that of dexmedetomidine pretreatment, which increased the expression of tight junction proteins, but it decreased the levels of DAO, D-LA, FABP2, and endotoxin. Moreover, the results demonstrated that due to pre-administration of dexmedetomidine, the level of pro-inflammatory factors was decreased, while the level of anti-inflammatory cytokine was increased. Also, it showed that dexmedetomidine suppressed TLR4/JAK2/STAT3 pathway that was activated by cardiopulmonary bypass. Together, these results revealed that dexmedetomidine pretreatment relieves intestinal microcirculation, attenuates intestinal damage, and inhibits the inflammatory response of cardiopulmonary bypass model rats, demonstrating that in CPB-induced damage of intestinal mucosal barrier function, dexmedetomidine pretreatment plays a protective role by inactivating TLR4/JAK2/STAT3-mediated inflammatory pathway.

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