Tannins extract from Galla Chinensis can protect mice from infection by Enterotoxigenic Escherichia coli O101

Abstract Background Enterotoxigenic Escherichia coli (ETEC) is classically associated with acute secretory diarrhea, which induces 2 million people death in developing countries over a year, predominantly children in the first years of life. Previously, tannins (47.75%) were extracted from Galla Chinensis and prepared as Galla Chinensis oral solution (GOS) which showed significant antidiarrheal activity in a castor oil-induced diarrhea in mice. Whether the tannins extract were also effective in treatment of ETEC-induced diarrhea was determined in this study. Methods Mice were randomly divided into 6 groups (n = 22). The mice in the normal and untreated groups were given normal saline. Three GOS-treated groups were received different concentrations of GOS (5, 10 and 15%, respectively) at a dose of 10 mL/kg. Mice in the positive control group were fed with loperamide (10 mg/kg). The treatment with GOS started 3 days before infection with ETEC and continued for 4 consecutive days after infection. On day 3, mice were all infected with one dose of LD50 of ETEC, except those in the normal group. Survival of mice was observed daily and recorded throughout the study. On days 4 and 7, samples were collected from 6 mice in each group. Results GOS could increase the survival rate up to 75%, while in the untreated group it is 43.75%. The body weights of mice treated with 15% GOS were significantly increased on day 7 in comparison with the untreated group and the normal group. GOS-treatment recovered the small intestine coefficient enhanced by ETEC-infection. The diarrhea index of mice treated with GOS was significantly decreased. GOS increased the levels of IgG and sIgA in the terminal ileum and decreased the levels of pro-inflammatory cytokines (IFN-γ, TNF-α, IL-1β, IL-6 and IL-8) in serum. GOS could increase the amount of intestinal probiotics, Lactobacilli and Bifidobacteria. GOS could alleviate colon lesions induced by ETEC-infection. GOS showed higher potency than loperamide. Conclusions GOS could be a promising drug candidate for treating ETEC infections.

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Lasso Peptide Microcin J25 Effectively Enhances Gut Barrier Function and Modulates Inflammatory Response in an Enterotoxigenic Escherichia coli-Challenged Mouse Model

International Journal of Molecular Sciences ◽

10.3390/ijms21186500 ◽

2020 ◽

Vol 21 (18) ◽

pp. 6500 ◽

Cited By ~ 1

Author(s):

Xiuliang Ding ◽

Haitao Yu ◽

Shiyan Qiao

Keyword(s):

Escherichia Coli ◽

Barrier Function ◽

Inflammatory Responses ◽

Intestinal Morphology ◽

Enterotoxigenic Escherichia Coli ◽

Control Group ◽

Lasso Peptide ◽

Gut Barrier Function ◽

Microcin J25 ◽

Etec Infection

Bacterial resistance leads to severe public health and safety issues worldwide. Alternatives to antibiotics are currently needed. A promising lasso peptide, microcin J25 (MccJ25), is considered to be the best potential substitute for antibiotics to treat pathogen infection, including enterotoxigenic Escherichia coli (ETEC). This study evaluated the efficacy of MccJ25 in the prevention of ETEC infection. Forty-five female BALB/c mice of clean grade (aged seven weeks, approximately 16.15 g) were randomly divided into three experimental groups as follows: (i) control group (uninfected); (ii) ETEC infection group; (iii) MccJ25 + ETEC group. Fifteen mice per group in five cages, three mice/cage. MccJ25 conferred effective protection against ETEC-induced body weight loss, decrease in rectal temperature and increase in diarrhea scores in mice. Moreover, in ETEC-challenged mice model, MccJ25 significantly improved intestinal morphology, decreased intestinal histopathological scores and attenuated intestinal inflammation by decreasing proinflammatory cytokines and intestinal permeability, including reducing serum diamine oxidase and D-lactate levels. MccJ25 enhanced epithelial barrier function by increasing occludin expression in the colon and claudin-1 expression in the jejunum, ultimately improving intestinal health of host. MccJ25 was further found to alleviate gut inflammatory responses by decreasing inflammatory cytokine production and expression via the activation of the mitogen-activated protein kinase and nuclear factor κB signaling pathways. Taken together, the results indicated that MccJ25 protects against ETEC-induced intestinal injury and intestinal inflammatory responses, suggesting the potential application of MccJ25 as an excellent antimicrobial or anti-inflammation agent against pathogen infections.

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Mouse duodenum as a model of inflammation induced by enterotoxigenic Escherichia coli K88

Journal of Veterinary Research ◽

10.1515/jvetres-2016-0004 ◽

2016 ◽

Vol 60 (1) ◽

pp. 19-23 ◽

Cited By ~ 6

Author(s):

Kai Wang ◽

Yu Qi ◽

Shushuai Yi ◽

Zhihua Pei ◽

Na Pan ◽

...

Keyword(s):

Escherichia Coli ◽

Clinical Symptoms ◽

Treated Group ◽

Model Material ◽

The Body ◽

Enterotoxigenic Escherichia Coli ◽

Control Group ◽

Mucous Layer ◽

E Coli ◽

Tnf Α

Abstract Introduction: The aim of the experiment was to establish the enterotoxigenic Escherichia coli K88 (ETEC K88)-induced BALB/c mouse duodenum inflammation model. Material and Methods: Mice were administered different concentrations of E. coli K88 (1.0 × 107-109 CFU/mL) for 3 d by means of an esophageal catheter. Results: The results showed that the treated group expressed several significant clinical symptoms, such as reduced dietary demands and weight loss, an increased presence of IL-1α, TNF-α, and MPO in the peripheral blood, and some pathological changes in the duodenum. On the 6th-8th days, the body weight of the mice was the lowest. On the 8th day, there were significant differences in IL-1α, TNF-α, and MPO levels compared to the control group (P < 0.05), the gap between the duodenum mucous layer and the muscular layer had widened, the number of goblet cells was increased, and the inflammatory infiltrate and inflammation changes in the lamina propria and the mucous layer were the most obvious. Conclusion: The duodenum inflammation was the most severe on day 8; thus, the model was successfully established. In addition, varying concentrations of ETEC K88 did not significantly influence the duodenum inflammation (P > 0.05).

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Immunogenicity and protective efficacy of enterotoxigenic Escherichia coli (ETEC) total RNA against ETEC challenge in a mouse model

Scientific Reports ◽

10.1038/s41598-020-77551-8 ◽

2020 ◽

Vol 10 (1) ◽

Author(s):

Mandi Liu ◽

Yue Zhang ◽

Di Zhang ◽

Yun Bai ◽

Guomei Liu ◽

...

Keyword(s):

Escherichia Coli ◽

Mouse Model ◽

Immune Responses ◽

Protective Efficacy ◽

Enterotoxigenic Escherichia Coli ◽

Economic Losses ◽

Th2 Response ◽

Total Rna ◽

Etec Infection

AbstractEnterotoxigenic Escherichia coli (ETEC), an essential cause of post-weaning diarrhea (PWD) in piglets, leads to significant economic losses to the pig industry. The present study aims to identify the role of ETEC total RNA in eliciting immune responses to protect animals against ETEC infection. The results showed that the total RNA isolated from pig-derived ETEC K88ac strain effectively stimulated the IL-1β secretion of porcine intestinal epithelial cells (IPEC-J2). The mouse model immunized with ETEC total RNA via intramuscular injection (IM) or oral route (OR) was used to evaluate the protective efficiency of the ETEC total RNA. The results suggested that 70 μg ETEC total RNA administered by either route significantly promoted the production of the serum IL-1β and K88ac specific immunoglobulins (IgG, IgM, and IgA). Besides, the ETEC RNA administration augmented strong mucosal immunity by elevating K88ac specific IgA level in the intestinal fluid. Intramuscularly administered RNA induced a Th1/Th2 shift toward a Th2 response, while the orally administered RNA did not. The ETEC total RNA efficiently protected the animals against the ETEC challenge either by itself or as an adjuvant. The histology characterization of the small intestines also suggested the ETEC RNA administration protected the small intestinal structure against the ETEC infection. Particularly of note was that the immunity level and protective efficacy caused by ETEC RNA were dose-dependent. These findings will help understand the role of bacterial RNA in eliciting immune responses, and benefit the development of RNA-based vaccines or adjuvants.

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The dietary arachidonic acid improved growth and immunity of honey bee (Apis mellifera ligustica)

Bulletin of Entomological Research ◽

10.1017/s0007485321000821 ◽

2021 ◽

pp. 1-10

Author(s):

Jing Yu ◽

Weixing Zhang ◽

Xuepeng Chi ◽

Wenfeng Chen ◽

Zhenfang Li ◽

...

Keyword(s):

Escherichia Coli ◽

Arachidonic Acid ◽

Apis Mellifera ◽

The Body ◽

Control Group ◽

Immune Functions ◽

Pufa Content ◽

Apis Mellifera Ligustica ◽

Immune Genes ◽

Mrna Expression Levels

Abstract Honeybees cannot synthesize arachidonic acid (ARA) themselves, only obtain it from food. Most pollen is deficient or contains a small amount of ARA. The necessity of supplementary ARA in bees’ diet has not been studied. The objective of this study was to investigate the effects of dietary ARA levels on the growth and immunity of Apis mellifera ligustica. A total of 25 honeybee colonies were randomly assigned to five dietary groups which were fed basic diets supplemented with 0, 2, 4, 6, and 8% of ARA. The diet with 4% ARA improved the body weight of newly emerged worker bees compared with the control group. Supplement of ARA in honeybee diets changed the fatty acid composition of honeybee body. SFA and MUFA contents of bees’ body declined, and PUFA content rised in the ARA group. Compared with the control group, the supplement of ARA in honeybee diets increased the contents of ARA, C22:6n-3 (DHA) and C18:3n-6 in bees’ body significantly, but decreased the contents of C16:1 and C18:3n-3. The diet supplied with 4% ARA reduced the mortality rate of honeybee infected with Escherichia coli. The activity of immune enzymes (phenoloxidase, antitrypsin, and lysozyme) and the mRNA expression levels of immune genes (defensin-2, toll, myd88, and dorsal) were improved by ARA diets to varying degrees depending on the ARA levels, especially 4% ARA. These results suggested that dietary ARA could improve the growth, survival, and immune functions of honeybees. Supplement of ARA in bees’ diet would be valuable for the fitness of honeybees.

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Enterotoxigenic Escherichia coli infection and intestinal thiamin uptake: studies with intestinal epithelial Caco-2 monolayers

AJP Cell Physiology ◽

10.1152/ajpcell.00276.2013 ◽

2013 ◽

Vol 305 (11) ◽

pp. C1185-C1191 ◽

Cited By ~ 8

Author(s):

Abhisek Ghosal ◽

Nabendu S. Chatterjee ◽

Tristan Chou ◽

Hamid M. Said

Keyword(s):

Escherichia Coli ◽

Significant Inhibition ◽

Water Soluble ◽

Enterotoxigenic Escherichia Coli ◽

Adenylate Cyclase System ◽

Mrna Levels ◽

Intestinal Epithelial ◽

E Coli ◽

Heat Labile ◽

Etec Infection

Infections with enteric pathogens like enterotoxigenic Escherichia coli ( ETEC) is a major health issue worldwide and while diarrhea is the major problem, prolonged, severe, and dual infections with multiple pathogens may also compromise the nutritional status of the infected individuals. There is almost nothing currently known about the effect of ETEC infection on intestinal absorptions of water-soluble vitamins including thiamin. We examined the effect of ETEC infection on intestinal uptake of the thiamin using as a model the human-derived intestinal epithelial Caco-2 cells. The results showed that infecting confluent Caco-2 monolayers with live ETEC (but not with boiled/killed ETEC or nonpathogenic E. coli) or treatment with bacterial culture supernatant led to a significant inhibition in thiamin uptake. This inhibition appears to be caused by a heat-labile and -secreted ETEC component and is mediated via activation of the epithelial adenylate cyclase system. The inhibition in thiamin uptake by ETEC was associated with a significant reduction in expression of human thiamin transporter-1 and -2 (hTHTR1 and hTHTR2) at the protein and mRNA levels as well as in the activity of the SLC19A2 and SLC19A3 promoters. Dual infection of Caco-2 cells with ETEC and EPEC (enteropathogenic E. coli) led to compounded inhibition in intestinal thiamin uptake. These results show for the first time that infection of human intestinal epithelial cells with ETEC causes a significant inhibition in intestinal thiamin uptake. This inhibition is mediated by a secreted heat-labile toxin and is associated with a decrease in the expression of intestinal thiamin transporters.

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Effect of Puerarin, Baicalin and Berberine Hydrochloride on the Regulation of IPEC-J2 Cells Infected with Enterotoxigenic Escherichia coli

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2019/7438593 ◽

2019 ◽

Vol 2019 ◽

pp. 1-15 ◽

Cited By ~ 3

Author(s):

Xiaoxi Liu ◽

Fenghua Liu ◽

Yunfei Ma ◽

Huanrong Li ◽

Xianghong Ju ◽

...

Keyword(s):

Escherichia Coli ◽

Inflammatory Response ◽

Signaling Pathway ◽

Bacterial Adhesion ◽

Inflammatory Responses ◽

Enterotoxigenic Escherichia Coli ◽

Intestinal Epithelial ◽

Berberine Hydrochloride ◽

Main Components ◽

Etec Infection

Puerarin, baicalin and berberine hydrochloride are the main components of Gegen Qinlian Decoction, which has been used to treat diarrhoea in China for hundreds of years, yet the biological function and molecular mechanism of these components are not clear. To investigate the effects of puerarin, baicalin, and berberine hydrochloride on the regulation of porcine intestinal epithelial cells (IPEC-J2 cells) infected with enterotoxigenic Escherichia coli (ETEC). IPEC-J2 cells were pretreated with puerarin (200 μg/mL), baicalin (1 μg/mL), and berberine hydrochloride (100 μg/mL) at 37°C for 3 h and then coincubated with the F4ac ETEC bacterial strain 200 at 37°C for 3 h. ETEC infection damaged the structure of IPEC-J2 cells, upregulated mucin 4 (P < 0.01) and mucin 13 mRNA (P < 0.05) expression, increased the apoptosis rate (P < 0.05), and promoted inflammatory responses (IL-6 and CXCL-2 mRNA expression) in IPEC-J2 cells by activating the nuclear factor-κB (NF-κB) signaling pathway. Pretreatment with puerarin, baicalin, and berberine hydrochloride improved the structure and morphology of IPEC-J2 cells and inhibited ETEC adhesion by downregulating specific adhesion molecules. Pretreatment with baicalin decreased the inflammatory response; pretreatment with baicalin and berberine hydrochloride decreased the inflammatory response mediated by the NF-κB signaling pathway. Pretreatment with puerarin, baicalin, and berberine hydrochloride protected IPEC-J2 cells from ETEC infection by inhibiting bacterial adhesion and inflammatory responses.

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First Characterization of Bioactive Components in Soybean Tempe That Protect Human and Animal Intestinal Cells against Enterotoxigenic Escherichia coli (ETEC) Infection

Journal of Agricultural and Food Chemistry ◽

10.1021/jf101379y ◽

2010 ◽

Vol 58 (13) ◽

pp. 7649-7656 ◽

Cited By ~ 13

Author(s):

Petra J. Roubos-van den Hil ◽

Henk A. Schols ◽

M. J. Rob Nout ◽

Marcel H. Zwietering ◽

Harry Gruppen

Keyword(s):

Escherichia Coli ◽

Enterotoxigenic Escherichia Coli ◽

Intestinal Cells ◽

Bioactive Components ◽

Etec Infection

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Screening of pigs resistant to F4 enterotoxigenic Escherichia coli (ETEC) infection

Veterinary Microbiology ◽

10.1016/j.vetmic.2007.02.017 ◽

2007 ◽

Vol 123 (1-3) ◽

pp. 249-253 ◽

Cited By ~ 39

Author(s):

K. Rasschaert ◽

F. Verdonck ◽

B.M. Goddeeris ◽

L. Duchateau ◽

E. Cox

Keyword(s):

Escherichia Coli ◽

Enterotoxigenic Escherichia Coli ◽

Etec Infection

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An outbreak of enterotoxigenic Escherichia coli (ETEC) infection in Norway, 2012: a reminder to consider uncommon pathogens in outbreaks involving imported products

Epidemiology and Infection ◽

10.1017/s0950268814001058 ◽

2014 ◽

Vol 143 (3) ◽

pp. 486-493 ◽

Cited By ~ 13

Author(s):

E. MacDONALD ◽

K. E. MØLLER ◽

A. L. WESTER ◽

U. R. DAHLE ◽

N. O. HERMANSEN ◽

...

Keyword(s):

Escherichia Coli ◽

Food Safety ◽

Confidence Interval ◽

Odds Ratio ◽

Enterotoxigenic Escherichia Coli ◽

Gastrointestinal Pathogens ◽

Heat Treated ◽

Sources Of Infection ◽

Initial Interviews ◽

Etec Infection

SUMMARYWe investigated an outbreak of gastroenteritis following a Christmas buffet served on 4–9 December 2012 to ~1300 hotel guests. More than 300 people were reported ill in initial interviews with hotel guests. To identify possible sources of infection we conducted a cohort investigation through which we identified 214 probable cases. Illness was associated with consumption of scrambled eggs (odds ratio 9·07, 95% confidence interval 5·20–15·84). Imported chives added fresh to the scrambled eggs were the suspected source of the outbreak but were unavailable for testing. Enterotoxigenic Escherichia coli (ETEC) infection was eventually confirmed in 40 hotel guests. This outbreak reinforces that ETEC should be considered in non-endemic countries when the clinical picture is consistent and common gastrointestinal pathogens are not found. Following this outbreak, the Norwegian Food Safety Authority recommended that imported fresh herbs should be heat-treated before use in commercial kitchens.

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