Protective effects of Lactobacillus plantarum on epithelial barrier disruption caused by enterotoxigenic Escherichia coli in intestinal porcine epithelial cells

Wu, Yunpeng; Zhu, Cui; Chen, Zhuang; Chen, Zhongjian; Zhang, Weina; Ma, Xianyong; Wang, Li; Yang, Xuefen; Jiang, Zhonghong

doi:10.1016/j.vetimm.2016.03.005

Cited by 113 publications

(104 citation statements)

References 41 publications

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“…This finding is consistent with L. reuteri I5007 increasing expression of ZO-1 and occludin in similar intestinal porcine epithelial cells (IPEC-J2) [14]. Another probiotic, L. plantarum , ameliorated disruptions of ZO-1 and occludin in IPEC-J2 cells caused by ETEC K88 challenge [30]. Moreover, L. acidophilus and Streptococcus thermophilus attenuated decreases in ZO-1 expression in intestinal epithelial cells caused by enteroinvasive E.coli [32].…”

Section: Discussionsupporting

confidence: 76%

“…The most important TJ proteins in the intestinal mucosa are ZO-1, occludin, and claudins [7], and the expression of all 3 in the intestine are decreased by infection with ETEC K88 [24, 30]. The present study showed that, for ZO-1 and occludin in IPEC-1 monolayers, this decrease from ETEC K88 infection was partially prevented by L. reuteri LR1.…”

Section: Discussionsupporting

confidence: 50%

“…Although the regulatory mechanism of beneficial probiotics on the intestinal epithelial barrier is still unclear, it is established that some probiotics do improve barrier function, thereby maintaining intestinal homeostasis [27–30]. L. reuteri LR1, a new strain isolated from the feces of a healthy weaning piglet, exhibits both probiotic and functional properties in porcine intestinal epithelial cells [24].…”

Section: Discussionmentioning

confidence: 99%

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Lactobacillus reuteri LR1 Improved Expression of Genes of Tight Junction Proteins via the MLCK Pathway in IPEC-1 Cells during Infection with Enterotoxigenic Escherichia coli K88

Wang

Xiong

et al. 2018

Mediators of Inflammation

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Intestinal epithelial barrier damage disrupts immune homeostasis and leads to many intestinal disorders. Lactobacillus reuteri strains have probiotic functions in their modulation of the microbiota and immune system in intestines. In this study, the effects of L. reuteri LR1, a new strain isolated from the feces of weaning piglets, on intestinal epithelial barrier damage in IPEC-1 cells caused by challenge with enterotoxigenic Escherichia coli (ETEC) K88 were examined. It was found that L. reuteri LR1, in large part, offset the ETEC K88-induced increase in permeability of IPEC-1 cell monolayers and decreased the adhesion and invasion of the coliform in IPEC-1 cells. In addition, L. reuteri LR1 increased transcript abundance and protein contents of tight junction (TJ) proteins zonula occluden-1 (ZO-1) and occludin in ETEC K88-infected IPEC-1 cells, whereas it had no effects on claudin-1 and F-actin expression. Using colloidal gold immunoelectron microscopy, these effects of L. reuteri LR1 on ZO-1 and occludin content in IPEC-1 cells were confirmed. By using ML-7, a selective inhibitor of myosin light-chain kinase (MLCK), the beneficial effect of L. reuteri LR1 on contents of ZO-1 and occludin was shown to be dependent on the MLCK pathway. In conclusion, L. reuteri LR1 had beneficial effects on epithelial barrier function consistent with increasing ZO-1 and occludin expression via a MLCK-dependent manner in IPEC-1 cells during challenge with ETEC K88.

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Section: Discussionsupporting

confidence: 76%

Section: Discussionsupporting

confidence: 50%

Section: Discussionmentioning

confidence: 99%

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Lactobacillus reuteri LR1 Improved Expression of Genes of Tight Junction Proteins via the MLCK Pathway in IPEC-1 Cells during Infection with Enterotoxigenic Escherichia coli K88

Wang

Xiong

et al. 2018

Mediators of Inflammation

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“…Wu et al [54] shows Lactobacillus plantarum may maintain TEER, inhibit the reduction of TJ proteins and reduce the expression of proinflammatory cytokines induced by ETEC K88 via modulation of TLRs, NF-κB and MAPK pathways, thus improving epithelial barrier. Some probiotic species appear to activate specific TLRs to influence the host cells [55, 56] .…”

Section: Molecular Mechanisms Of Probiotics In Gi Diseasesmentioning

confidence: 99%

Vitamin D/VDR, Probiotics, and Gastrointestinal Diseases

Shang

Sun

2017

CMC

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Vitamin D is an important factor in regulating inflammation, immune responses, and carcinoma inhibition via action of its receptor, vitamin D receptor (VDR). Recent studies have demonstrated the role of vitamin D/VDR in regulating host-bacterial interactions. Probiotics are beneficial bacteria with the power of supporting or favoring life on the host. In the current review, we will discuss the recent progress on the roles of vitamin D/VDR in gut microbiome and inflammation. We will summarize evidence of probiotics in modulating vitamin D/VDR and balancing gut microbiota in health and gastrointestinal diseases. Moreover, we will review the clinical application of probiotics in prevention and therapy of IBD or colon cancer. Despite of the gains, there remain several barriers to advocate broad use of probiotics in clinical therapy. We will also discuss the limits and future direction in scientific understanding of probiotics, vitamin D/VDR, and host responses.

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“…Successful early strategies to enhance the level of colonization resistance used supplementation with core probiotic bacteria, a process sometimes called competitive exclusion or Nurmi Concept, to first overcome a 1970s outbreak of salmonellosis in poultry and later for other pathogens (Nurmi et al 1992;Neal-McKinney et al 2012). Similar strategies have been applied for other sectors of agriculture where useful outcomes can be measured as reduced infections or pathogen burden, improved barrier function, reduced inflammation, and even enhanced nutrient utilization and/or growth (Pollmann et al 2005;Hai 2015;Angelakis et al 2016;Wu et al 2016).…”

Section: Embracing Colonization Resistancementioning

confidence: 99%

Safety and risk assessment for the human superorganism

Dietert

2017

Human and Ecological Risk Assessment: An International Journal

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This editorial on safety evaluation and risk assessment for the human superorganism introduces a series of papers arguing for a fundamental shift in how we approach human health risk assessment. In this series emphasis is placed on the risk of infectious disease. Our 21 st st century understanding of human biology is that, as holobionts, we possess a majority of microbial cells and genes. In fact, our microbes fundamentally affect our interactions with the external environment, metabolism, physiology, and risk of both pathology and disease. As holobionts, we require our microbial partners for us to be both complete and healthy. Using the 20 th century understanding of human biology, we failed to capture the effects of the microbiome in evaluating health risks. But 21 st century risk assessments such as those associated with exposure to specific microbial pathogens need to include the human microbiome. Microbiome status will be central in determining the health risks for both individuals and populations.

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Protective effects of Lactobacillus plantarum on epithelial barrier disruption caused by enterotoxigenic Escherichia coli in intestinal porcine epithelial cells

Cited by 113 publications

References 41 publications

Lactobacillus reuteri LR1 Improved Expression of Genes of Tight Junction Proteins via the MLCK Pathway in IPEC-1 Cells during Infection with Enterotoxigenic Escherichia coli K88

Lactobacillus reuteri LR1 Improved Expression of Genes of Tight Junction Proteins via the MLCK Pathway in IPEC-1 Cells during Infection with Enterotoxigenic Escherichia coli K88

Vitamin D/VDR, Probiotics, and Gastrointestinal Diseases

Safety and risk assessment for the human superorganism

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