<i>Enterococcus faecium</i>HDRsEf1 elevates the intestinal barrier defense against enterotoxigenic<i>Escherichia coli</i>and regulates occludin expression via activation of TLR-2 and PI3K signalling pathways

Yan, Tiekun; Zhang, F.; He, Yan; Wang, Xianwei; Jin, Xiaodong; Zhang, P.; Bi, Dingren

doi:10.1111/lam.13067

Cited by 16 publications

(18 citation statements)

References 27 publications

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“…Enhanced tight junctions following E. faecium supplementation resulted in reduced gut permeability and reduced pathogen invasion. In accordance with our findings, several other studies have shown that probiotic E. faecium reinforced epithelial barrier function in pigs and mice with intestinal inflammation 19,49,50 and prevented Enterotoxigenic E . coli ( ETEC )-induced reductions in CLDN-1 mRNA and protein levels in pig cell models 26–28 .…”

Section: Discussionsupporting

confidence: 93%

Pretreatment with probiotic Enterococcus faecium NCIMB 11181 ameliorates necrotic enteritis-induced intestinal barrier injury in broiler chickens

Zhen

Geng

et al. 2019

Sci Rep

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The dysfunction of tight-junction integrity caused by necrotic enteritis (NE) is associated with decreased nutrient absorption and gut injury in broiler chickens. Although probiotic Enterococcus faecium ( E. faecium ) has been reported to possess immune-regulatory characteristics and can prevent diarrhea in pigs, very little information exists in relation to the specific regulatory impact of E. faecium NCIMB 11181 on NE-induced intestinal barrier injury of broiler chickens. This study was conducted to investigate the protective effects of probiotic E. faecium NCIMB 11181 on NE-induced intestinal barrier injury in broiler chickens. The study also aimed to elucidate the mechanisms that underpin these protective effects. One hundred and eighty Arbor Acres (AA) broiler chicks (one day old) were randomly assigned using a 2 × 2 factorial arrangement into two groups fed different levels of dietary E. faecium NCIMB 11181 (0 or 2 × 10 8 CFU/kg of diet) and two disease-challenge groups (control or NE challenged). The results showed that NE induced body weight loss, intestinal lesions, and histopathological inflammation, as well as intestinal-cell apoptosis. These symptoms were alleviated following the administration of probiotic E. faecium NCIMB 11181. Pretreatment with probiotic E. faecium NCIMB 11181 significantly upregulated the expression of the Claudin-1 gene encoding a tight-junction protein. Claudin-1 and HSP70 protein expression were also increased in the jejunum regardless of NE infection. Furthermore, NE-infected birds fed with E. faecium displayed notable increases in MyD88, NF-κB, iNOS, PI3K, GLP-2, IL-1β, IL-4, and HSP70 mRNA expression. E. faecium NCIMB 11181 administration also significantly improved the animals’ intestinal microbial composition regardless of NE treatment. These findings indicated that addition of E. faecium NCIMB 11181 to poultry feed is effective in mitigating NE-induced gut injury, possibly by strengthening intestinal mucosal barrier function, as well as modulating gut microflora and intestinal mucosal immune responses.

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Section: Discussionsupporting

confidence: 93%

Pretreatment with probiotic Enterococcus faecium NCIMB 11181 ameliorates necrotic enteritis-induced intestinal barrier injury in broiler chickens

Zhen

Geng

et al. 2019

Sci Rep

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“…Actually, A20 is a deubiquitinating enzyme and can inhibit the NF-kB activation (Boone et al, 2004). Our previous study indicates that Enterococcus faecium HDRsEf1 enhances the expression of occluding, the intestinal tight junction protein, by activating the TLR2 (Yan et al, 2018). Accordingly, we hypothesize that HDRsEf1 can modulate the expression of CYP3A29 in pig intestinal tissues by modulating the NB-kB signaling.…”

Section: Introductionmentioning

confidence: 92%

“…Bacterial preparations, cell culture and treatment Enterococcus faecium HDRsEf1 is novel probiotic strain (CCTCC NO: M2011031) (Yan et al, 2018). The HDRsEf1 bacteria were grown in De Man Rogosa Sharpe (MRS) media (Difco, Sparks, USA) at 37 °C for 18 h,and collected by centrifugation.…”

Section: Special Chemicals and Reagentsmentioning

confidence: 99%

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Enterococcus faecium HDRsEf1 Represses CYP3A29 Expression in the Intestine through the TLR1/2-induced A20 to attenuate the NF-κB/RXR-α Signaling

Gong

et al. 2020

Preprint

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Background CYP3A29 is crucial for drug metabolism in pigs and an important research model of human CYP3A4. Recent studies have shown that some probiotics can regulate the expression of CYP3A in mammals, but the mechanisms underlying their action are unclear. This study explored whether Enterococcus faecium HDRsEf1 could modulate the expression of CYP3A29 in pig intestine and potential mechanisms. Results we found that HDRsEf1 significantly reduced CYP3A29 expression in pig intestinal tissues and epithelial cells, dependent on cell-cell contact. In IPEC-J2 cells, HDRsEf1 treatment decreased the transcription activity of the CYP3A29 promoter, RXR-α expression and abrogated or mitigated the RXR-α or PXR over-expression-increased CYP3A29 expression. Both RXR-α/PXR over-expression synergistically increased CYP3A29 expression while RXR-α or PXR silencing reduced CYP3A29 expression. Co-immunoprecipitation revealed that RXR-α directly interacted with PXR. HDRsEf1, like a NF-kB inhibitor, significantly decreased the NF-kBp65 activation, RXR-α and CYP3A29 expression, which were abrogated by RXR-α silencing. The down-regulated CYP3A29 expression by HDRsEf1 was associated with increased A20 expression, which were abrogated by TLR1/2 silencing. Conclusions HDRsEf1 inhibits the expression of CYP3A29 through the TLR1/2-induced A20 to attenuate the NF-κB/RXR-α signaling in pig intestinal tissues. Our findings may provide new insights into the mechanisms by which probiotics regulate the expression of CYP450s, and suggest potential risks in the clinical application of probiotics

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“…Enterotoxigenic Escherichia coli (ETEC) are commonly associated with post-weaning diarrhea (PWD) in piglets, a disease causing serious losses in the pig industry worldwide (Fairbrother et al, 2005; Rhouma et al, 2017a). Currently, different strategies are utilized to reduce ETEC-associated economic costs in pig farming, including oral colistin sulfate treatment in some regions of the world (Rhouma et al, 2017b), vaccination (Moon and Bunn, 1993; Blázquez et al, 2018) and probiotics (Li et al, 2018; Yan et al, 2018). In addition, high-level dietary zinc oxide supplementation is used against PWD in the pig production sector (Fairbrother et al, 2005; Vahjen et al, 2011; Bednorz et al, 2013; Starke et al, 2014; Pieper et al, 2015; Kloubert et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Effects of a Four-Week High-Dosage Zinc Oxide Supplemented Diet on Commensal Escherichia coli of Weaned Pigs

et al. 2019

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Strategies to reduce economic losses associated with post-weaning diarrhea in pig farming include high-level dietary zinc oxide supplementation. However, excessive usage of zinc oxide in the pig production sector was found to be associated with accumulation of multidrug resistant bacteria in these animals, presenting an environmental burden through contaminated manure. Here we report on zinc tolerance among a random selection of intestinal Escherichia coli comprising of different antibiotic resistance phenotypes and sampling sites isolated during a controlled feeding trial from 16 weaned piglets: In total, 179 isolates from “pigs fed with high zinc concentrations” (high zinc group, [HZG]: n = 99) and a corresponding “control group” ([CG]: n = 80) were investigated with regard to zinc tolerance, antimicrobial- and biocide susceptibilities by determining minimum inhibitory concentrations (MICs). In addition, in silico whole genome screening (WGSc) for antibiotic resistance genes (ARGs) as well as biocide- and heavy metal tolerance genes was performed using an in-house BLAST-based pipeline. Overall, porcine E. coli isolates showed three different ZnCl2 MICs: 128 μg/ml (HZG, 2%; CG, 6%), 256 μg/ml (HZG, 64%; CG, 91%) and 512 μg/ml ZnCl2 (HZG, 34%, CG, 3%), a unimodal distribution most likely reflecting natural differences in zinc tolerance associated with different genetic lineages. However, a selective impact of the zinc-rich supplemented diet seems to be reasonable, since the linear mixed regression model revealed a statistically significant association between “higher” ZnCl2 MICs and isolates representing the HZG as well as “lower ZnCl2 MICs” with isolates of the CG (p = 0.005). None of the zinc chloride MICs was associated with a particular antibiotic-, heavy metal- or biocide- tolerance/resistance phenotype. Isolates expressing the 512 μg/ml MIC were either positive for ARGs conferring resistance to aminoglycosides, tetracycline and sulfamethoxazole-trimethoprim, or harbored no ARGs at all. Moreover, WGSc revealed a ubiquitous presence of zinc homeostasis and – detoxification genes, including zitB, zntA, and pit. In conclusion, we provide evidence that zinc-rich supplementation of pig feed selects for more zinc tolerant E. coli, including isolates harboring ARGs and biocide- and heavy metal tolerance genes – a putative selective advantage considering substances and antibiotics currently used in industrial pork production systems.

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Enterococcus faeciumHDRsEf1 elevates the intestinal barrier defense against enterotoxigenicEscherichia coliand regulates occludin expression via activation of TLR-2 and PI3K signalling pathways

Cited by 16 publications

References 27 publications

Pretreatment with probiotic Enterococcus faecium NCIMB 11181 ameliorates necrotic enteritis-induced intestinal barrier injury in broiler chickens

Pretreatment with probiotic Enterococcus faecium NCIMB 11181 ameliorates necrotic enteritis-induced intestinal barrier injury in broiler chickens

Enterococcus faecium HDRsEf1 Represses CYP3A29 Expression in the Intestine through the TLR1/2-induced A20 to attenuate the NF-κB/RXR-α Signaling

Effects of a Four-Week High-Dosage Zinc Oxide Supplemented Diet on Commensal Escherichia coli of Weaned Pigs

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