Basic and clinical research on the regulation of the intestinal barrier by Lactobacillus and its active protein components: a review with experience of one center

Liu, Zhihua; Kang, Liang; Wang, Jianping

doi:10.1007/s11033-014-3701-9

Cited by 10 publications

(7 citation statements)

References 88 publications

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“…In this context, Lactobacillus deficiency may contribute to the development of NSAID-enteropathy. Indeed, these probiotic bacteria exert a protective effect on the intestinal barrier and reduce intestinal permeability ( Mennigen and Bruewer, 2009 ; Liu et al, 2014 ), and several experimental and human studies (for review see Syer et al, 2015 ) have shown their ability to prevent NSAID-induced small bowel lesions.…”

Section: Discussionmentioning

confidence: 99%

Pathophysiology of NSAID-Associated Intestinal Lesions in the Rat: Luminal Bacteria and Mucosal Inflammation as Targets for Prevention

et al. 2018

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Non-steroidal anti-inflammatory drugs (NSAIDs) can damage the small intestine, mainly through an involvement of enteric bacteria. This study examined the pathophysiology of NSAID-associated intestinal lesions in a rat model of diclofenac-enteropathy and evaluated the effect of rifaximin on small bowel damage. Enteropathy was induced in 40-week old male rats by intragastric diclofenac (4 mg/kg BID, 14 days). Rifaximin (delayed release formulation) was administered (50 mg/kg BID) 1 h before the NSAID. At the end of treatments, parameters dealing with ileal damage, inflammation, barrier integrity, microbiota composition, and TLR-NF-κB-inflammasome pathway were evaluated. In addition, the modulating effect of rifaximin on NLRP3 inflammasome was tested in an in vitro cell system. Diclofenac induced intestinal damage and inflammation, triggering an increase in tissue concentrations of tumor necrosis factor and interleukin-1β, higher expression of TLR-2 and TLR-4, MyD88, NF-κB and activation of caspase-1. In addition, the NSAID decreased ileal occludin expression and provoked a shift of bacterial phyla toward an increase in Proteobacteria and Bacteroidetes abundance. All these changes were counterbalanced by rifaximin co-administration. This drug was also capable of increasing the proportion of Lactobacilli, a genus depleted by the NSAID. In LPS-primed THP-1 cells stimulated by nigericin (a model to study the NLRP3 inflammasome), rifaximin reduced IL-1β production in a concentration-dependent fashion, this effect being associated with inhibition of the up-stream caspase-1 activation. In conclusion, diclofenac induced ileal mucosal lesions, driving inflammatory pathways and microbiota changes. In conclusion, rifaximin prevents diclofenac-induced enteropathy through both anti-bacterial and anti-inflammatory activities.

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Section: Discussionmentioning

confidence: 99%

Pathophysiology of NSAID-Associated Intestinal Lesions in the Rat: Luminal Bacteria and Mucosal Inflammation as Targets for Prevention

et al. 2018

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“…Recent evidence revealed that beneficial probiotics show promise for the treatment of disorder of small intestinal contractile activity caused by TBI [ 33 ]. Lactobacillus is one of the predominant probiotics in the animal’s GI tract which are defined as live microorganisms and when administered in adequate amounts, confer a health benefit to the host [ 5 , 34 , 35 ]. Maasi M et al reported that the probiotic preparation VSL#3 (e.g.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Lactobacillus acidophilus on the Intestinal Smooth Muscle Contraction through PKC/MLCK/MLC Signaling Pathway in TBI Mouse Model

Sun¹,

Hu²,

Fang³

et al. 2015

PLoS ONE

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Clinical studies have shown that probiotics influence gastrointestinal motility. However, the molecular mechanisms by which probiotic Lactobacillus modulates intestinal motility in traumatic brain injury (TBI) mouse model have not been explored. In the present study, we provided evidence showing that treatment of TBI mice with Lactobacillus acidophilus significantly improved the terminal ileum villus morphology, restored the impaired interstitial cells of Cajal (ICC) and the disrupted ICC networks after TBI, and prevented TBI-mediated inhibition of contractile activity in intestinal smooth muscle. Mechanistically, the decreased concentration of MLCK, phospho-MLC20 and phospho-MYPT1 and increased concentration of MLCP and PKC were observed after TBI, and these events mediated by TBI were efficiently prevented by Lactobacillus acidophilus application. These findings may provide a novel mechanistic basis for the application of Lactobacillus acidophilus in the treatment of TBI.

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“…LP can improve intestinal pathological disorders through the modulation of intestinal functions [ 2 ]. Therefore, as one of the best-characterized probiotic bacteria, LP can be selected in clinical trials assessing the prevention and treatment of intestinal disorders, such as the complications after surgical operation [ 2 , 4 , 5 ]. However, which components mostly contribute to the protective effects of LP still remains an interesting question to be further investigated [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

Knockout of MIMP protein in lactobacillus plantarumlost its regulation of intestinal permeability on NCM460 epithelial cells through the zonulin pathway

Liu

Kang

et al. 2014

BMC Gastroenterol

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BackgroundPrevious studies indicated that the micro integral membrane protein located within the media place of the integral membrane protein of Lactobacillus plantarum CGMCC 1258 had protective effects against the intestinal epithelial injury. In our study, we mean to establish micro integral membrane protein -knockout Lactobacillus plantarum (LPKM) to investigate the change of its protective effects and verify the role of micro integral membrane protein on protection of normal intestinal barrier function.MethodsBinding assay and intestinal permeability were performed to verify the protective effects of micro integral membrane protein on intestinal permeability in vitro and in vivo. Molecular mechanism was also determined as the zonulin pathway. Clinical data were also collected for further verification of relationship between zonulin level and postoperative septicemia.ResultsLPKM got decreased inhibition of EPEC adhesion to NCM460 cells. LPKM had lower ability to alleviate the decrease of intestinal permeability induced by enteropathogenic-e.coli, and prevent enteropathogenic-e.coli -induced increase of zonulin expression. Overexpression of zonulin lowered the intestinal permeability regulated by Lactobacillus plantarum. There was a positive correlation between zonulin level and postoperative septicemia. Therefore, micro integral membrane protein could be necessary for the protective effects of Lactobacillus plantarum on intestinal barrier.ConclusionMIMP might be a positive factor for Lactobacillus plantarum to protect the intestinal epithelial cells from injury, which could be related to the zonulin pathway.

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Basic and clinical research on the regulation of the intestinal barrier by Lactobacillus and its active protein components: a review with experience of one center

Cited by 10 publications

References 88 publications

Pathophysiology of NSAID-Associated Intestinal Lesions in the Rat: Luminal Bacteria and Mucosal Inflammation as Targets for Prevention

Pathophysiology of NSAID-Associated Intestinal Lesions in the Rat: Luminal Bacteria and Mucosal Inflammation as Targets for Prevention

The Effects of Lactobacillus acidophilus on the Intestinal Smooth Muscle Contraction through PKC/MLCK/MLC Signaling Pathway in TBI Mouse Model

Knockout of MIMP protein in lactobacillus plantarumlost its regulation of intestinal permeability on NCM460 epithelial cells through the zonulin pathway

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