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Summary
The continuous monolayer of intestinal epithelial cells [IECs] lining the gut lumen functions as the site of nutrient absorption and as a physical barrier to prevent the translocation of microbes and associated toxic compounds into the peripheral vasculature [1]. IECs also express host defense proteins such as intestinal alkaline phosphatase [IAP], which detoxify bacterial products and prevent intestinal inflammation [2, 3, 4, 5]. Our laboratory recently showed that IAP is enriched on vesicles that are released from the tips of IEC microvilli and accumulate in the intestinal lumen [6, 7]. Here, we show that these native “lumenal vesicles” [LVs] [1] contain catalytically active IAP that can dephosphorylate lipopolysaccharide [LPS], [2] cluster on the surface of native lumenal bacteria, [3] prevent the adherence of enteropathogenic E. coli [EPEC] to epithelial monolayers, and [4] limit bacterial population growth. We also find that IECs upregulate LV production in response to EPEC and other Gram-negative pathogens. Together, these results suggest that microvillar vesicle shedding represents a novel mechanism for distributing host defense machinery into the intestinal lumen and that microvillus-derived LVs modulate epithelial-microbial interactions.
Highlights
► Enterocyte microvillus-derived lumenal vesicles [LVs] detoxify bacterial toxins ► LVs bind directly to bacteria and prevent pathogenic attachment to epithelial cells ► LVs limit population growth of both commensal and pathogenic bacteria ► LV production is a constitutive process but is upregulated by bacterial stimulation
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Review
Locus of enterocyte effacement: a pathogenicity island involved in the virulence of enteropathogenic and enterohemorragic Escherichia coli subjected to a complex network of gene regulation
Fernanda M Franzin et al. Biomed Res Int. 2015.
Free PMC article
Abstract
The locus of enterocyte effacement [LEE] is a 35.6 kb pathogenicity island inserted in the genome of some bacteria such as enteropathogenic Escherichia coli, enterohemorrhagic E.coli, Citrobacter rodentium, and Escherichia albertii. LEE comprises the genes responsible for causing attaching and effacing lesions, a characteristic lesion that involves intimate adherence of bacteria to enterocytes, a signaling cascade leading to brush border and microvilli destruction, and loss of ions, causing severe diarrhea. It is composed of 41 open reading frames and five major operons encoding a type three system apparatus, secreted proteins, an adhesin, called intimin, and its receptor called translocated intimin receptor [Tir]. LEE is subjected to various levels of regulation, including transcriptional and posttranscriptional regulators located both inside and outside of the pathogenicity island. Several molecules were described being related to feedback inhibition, transcriptional activation, and transcriptional repression. These molecules are involved in a complex network of regulation, including mechanisms such as quorum sensing and temporal control of LEE genes transcription and translation. In this mini review we have detailed the complex network that regulates transcription and expression of genes involved in this kind of lesion.
Figures
Schematic representation of LEE genes transcription regulation. The pointed arrows indicate activation, and repression is represented by blunt arrows.
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