Lactobacillus plantarum inhibits the intestinal epithelial migration of neutrophils induced by enteropathogenic Escherichia coli.

Department of Pediatrics, Division of Gastroenterology and Nutrition, Wright State University and The Children's Medical Center, Dayton, Ohio 45404, USA.
Journal of Pediatric Gastroenterology and Nutrition (Impact Factor: 2.2). 04/2003; 36(3):385-91.
Source: PubMed

ABSTRACT Lactobacillus plantarum is a Gram-positive bacillus known for its effect as a probiotic agent. The goal of the study was to determine whether L. plantarum is capable of inhibiting the transepithelial neutrophil migration induced by enteropathogenic Escherichia coli (EPEC).
Cultured intestinal epithelial T-84 cell monolayers were rapidly infected with EPEC. L. plantarum or culture supernatants were added to the monolayers before and after the infection. Indium-labeled neutrophils were added to the basolateral side of inverted monolayers. After 150-minute incubation, radioactivity of the neutrophils that migrated in the physiologic direction was assayed, and the number of migrating neutrophils was calculated. L. plantarum was also added to the monolayers before and after EPEC infection, and the number of adherent EPEC was determined by plate counting.
EPEC-induced neutrophil migration and EPEC binding to monolayers were inhibited by viable L. plantarum but only when added to the monolayers before EPEC. Culture supernatants failed to inhibit the neutrophil migration.
These results suggest that L. plantarum is beneficial in inhibiting neutrophil migration induced by EPEC, but only when preincubated with host epithelia. Rather than an indirect effect through a secreted substance produced by the probiotic agent, its effect is direct and requires the presence of the bacterium.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Upon ingestion, probiotics may act to protect the host through a number of protective mechanisms including modulation of genes involved in intestinal innate mucosal defense such as epithelial cell-derived mucin glycoproteins and inhibitor of apoptosis proteins. To determine the specificity of effect and sustainability of response in vivo, Lactobacillus plantarum 299v (Lp299v), Lactobacillus rhamnosus R0011 (LrR0011), and Bifidobacterium bifidum R0071 (BbR0071) were added repeatedly or intermittently to the drinking water of Sprague-Dawley rats. After killing the rats via CO2 suffocation, Muc2, Muc3, neuronal apoptosis inhibitor protein (NAIP), human inhibitor of apoptosis protein 1/cellular inhibitor of apoptosis 2 (HIAP1/cIAP2), and human inhibitor of apoptosis protein 2/cellular inhibitor of apoptosis 1 (HIAP2/cIAP1) mRNA and protein levels were analyzed via RT-PCR and immunohistochemistry. Live Lp299v, BbR0071, and LrR0011 increased Muc3 protein and mRNA expression in jejunum and ileum. Heat-killed and a nonadherent derivative of Lp299v failed to induce Muc3 expression. Lp299v did induce expression of HIAP2/cIAP1 and NAIP expression. Muc3 mucin expression was elevated for 5 d after oral administration of Lp299v; however, this effect was not sustained despite ongoing daily ingestion of a probiotic. Intermittent pulse ingestion of probiotics, however, was found to repeatedly increase Muc3 expression. We conclude that selected probiotics can induce protective genes of mucosal intestinal epithelial cells, an effect that is reproducible with pulse probiotic administration.
    Pediatric Research 03/2011; 69(3):206-11. · 2.67 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Selective microbes used as probiotics can enhance epithelial cell protection. We have previously shown that a Lactobacillus plantarum strain 299v (Lp299v) has the ability to induce mucin genes. In the current study, we utilized a cytokine model of inflammation in cell culture to study the modulation of apoptosis by this probiotic. HT-29 cells were pre-incubated with the Lp299v or L. plantarum strain adh- (Lpadh-), a non-adherent derivative of Lp299v. Cells were challenged with a mixture of cytokines (TNF-α, IFN-γ, and IL-1a) to imitate conditions of inflammation. To assess for cell death, we evaluated TUNEL, multi-caspase, and caspase-3 and caspase-7 activity assays. There was a marked decrease in apoptosis as measured by TUNEL+ cells in samples pre-treated with Lp299v (18.7 ± 4.1%, p p 0.05). Similarly, caspase-3, caspase-7 activity was also reduced by Lp299v. Selected probiotics may confer an exogenous protective effect at the mucosal–luminal interface for intestinal epithelial cells via alteration of caspase-dependent apoptotic pathways.
    Probiotics and Antimicrobial Proteins 01/2011; 3(1):21-26.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Irritable Bowel Syndrome (IBS) is a common condition that negatively impacts the quality of life for many individuals. The exact etiology of this disorder is largely unknown; however, emerging studies suggest that the gut microbiota is a contributing factor. Several clinical trials show that probiotics, such as VSL#3, can have a favorable effect on IBS. This double-blind, randomized placebo-controlled study has been conducted in diarrhea-predominant IBS subjects in order to investigate the effect of VSL#3 on the fecal microbiota. The bacterial composition of the fecal microbiota was investigated using high-throughput microarray technology to detect 16S RNA. Twenty four subjects were randomized to receive VSL#3 or placebo for 8 weeks. IBS symptoms were monitored using GSRS and quality of life questionnaires. A favorable change in Satiety subscale was noted in the VSL #3 groups. However, the consumption of the probiotic did not change the gut microbiota. There were no adverse events or any safety concerns encountered during this study. To summarize, the use of VSL#3 in this pilot study was safe and showed improvement in specific GSRS-IBS scores in diarrhea-predominant IBS subjects. The gut microbiota was not affected by VSL#3 consumption suggesting that the mechanism of action is not directly linked to the microbiota.
    Probiotics and Antimicrobial Proteins 03/2011; 3(1):1-7.