Lactobacillus plantarum MB452 enhances the function of the intestinal barrier by increasing the expression levels of genes involved in tight junction formation

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Authors: Rachel C. Anderson, Adrian L. Cookson, Warren C. McNabb, Zaneta Park, Mark J. McCann and William J. Kelly
Date: Dec. 9, 2010
From: BMC Microbiology(Vol. 10)
Publisher: BioMed Central Ltd.
Document Type: Report
Length: 7,067 words

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Authors: Rachel C Anderson (corresponding author) [1]; Adrian L Cookson [1]; Warren C McNabb [2,3]; Zaneta Park [4]; Mark J McCann [1]; William J Kelly [5]; Nicole C Roy [1,3]

Background

The intestinal barrier is the largest interface between man and the external environment, and the maintenance of its integrity has an important role in preserving health. When intestinal barrier function is compromised, it can become "leaky" allowing pathogens and toxins to enter the body. The function of the intestinal barrier is compromised in human conditions such as Inflammatory Bowel Diseases (Crohn's Disease and Ulcerative Colitis) [1], Irritable Bowel Syndrome [2] and some kinds of food-borne infections [3]. Moreover, intestinal barrier function can be temporarily impaired during times of stress [4] and it inevitably deteriorates with aging [5]. In addition, increased intestinal permeability can also result in pathological changes in distant organs and tissues, which can lead to further complications in susceptible individuals such as asthma [6], chronic heart failure [7], type-1-diabetes [8], chronic fatigue syndrome [9] and depression [10].

A critical component of the intestinal barrier is the intercellular junction complexes between adjacent intestinal epithelial cells which form a semi-permeable diffusion barrier. These intercellular complexes consist of tight junctions, adherens junctions, desmosomes and gap junctions [11]. The tight junctions are the most apical and are responsible for controlling the permeability of the paracellular pathway. Tight junctions are formed by protein dimers that span the space between adjacent cell membranes. There are over 40 proteins with well recognised roles in tight junction formation. These proteins can be divided into three functional categories: 1) bridge proteins which form a web between adjacent cell membranes; 2) plaque proteins which anchor bridge proteins to the actin cytoskeleton; and 3) dual location proteins which are not continuously associated with the tight junctions and also act as transcription factors.

The maintenance or enhancement of intestinal barrier function is a beneficial property that some probiotic bacteria exert. Some probiotics have been shown to ameliorate intestinal permeability induced by pathogens in vitro [12, 13]; whereas, others probiotic bacteria have been shown to enhance tight junction integrity between intestinal epithelial cells that are not weakened [13, 14, 15]. Existing mechanistic studies have focused on the ability of probiotics to prevent alterations to few tight junction bridging proteins in disease models, e.g. the effect of VSL#3 on dextran sodium sulphate-induced colitis in mice [16] and the effect of Lactobacillus plantarum CGMCC 1258 on Enteroinvasive E. coli ATCC 43893 (serotype O124:NM)-induced barrier disruption in vitro [17]. The effect of probiotics on tight junction proteins in a healthy intestinal barrier have not been reported, nor the effect of probiotic bacteria on epithelial cell genes involved in the whole tight junction signalling pathway, including those encoding for bridging, plaque and dual location tight junction proteins. Alteration of tight junction signalling in healthy humans is a potential mechanism that could lead to the strengthening of the intestinal barrier, resulting in limiting the ability of antigens to enter the body and potentially triggering undesirable immune responses.

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Source Citation

Source Citation
Anderson, Rachel C., et al. "Lactobacillus plantarum MB452 enhances the function of the intestinal barrier by increasing the expression levels of genes involved in tight junction formation." BMC Microbiology, vol. 10, 2010, p. 316. Accessed 16 Jan. 2021.
  

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