Comparative study of pathogenic and non-pathogenic Escherichia coli outer membrane vesicles and prediction of host-interactions with TLR signaling pathways

The intestine is the major defensive barrier in the body by having more than 60% of the immune cells in the intestinal mucosa. The aim of this study was to evaluate the Toll like receptor (TLR) signaling pathways and immune response profiles, against outer membrane vesicles (OMVs) in pathogenic and...

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Bibliographic Details
Published in:BMC research notes 2018-08, Vol.11 (1), p.539-539, Article 539
Main Authors: Behrouzi, Ava, Vaziri, Farzam, Riazi Rad, Farhad, Amanzadeh, Amir, Fateh, Abolfazl, Moshiri, Arfa, Khatami, Shohreh, Siadat, Seyed Davar
Format: Article
Language:English
Subjects:
Bacteria
Bacterial Outer Membrane Proteins - physiology
Cells
Cytokines
E coli
Epithelial Cells
Escherichia coli
Escherichia coli - physiology
Homeostasis
Humans
Immune response
Inflammation
Interleukin 10
Interleukin 17
Intestinal Mucosa
Intestine
Membrane vesicles
Microscopy
Outer membrane vesicles
Research Note
Signal Transduction
Signaling
Software
Tight junctions
Toll like receptor
Toll-like receptors
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Summary:The intestine is the major defensive barrier in the body by having more than 60% of the immune cells in the intestinal mucosa. The aim of this study was to evaluate the Toll like receptor (TLR) signaling pathways and immune response profiles, against outer membrane vesicles (OMVs) in pathogenic and non-pathogenic strains of Escherichia coli. Our results demonstrated that despite inducing inflammatory and regulatory responses to OMVs released by both strains, there is a remarkable difference in the nature and severity of these responses between the two strains. Following the production and release of OMV by the pathogenic strain, the expressions of the pro-inflammatory cytokines were significantly elevated, in comparison to the non-pathogenic strains. Eventually, our findings suggest that OMV released by the pathogen strain might be colonized, causing inflammation, eliminating the tight junctions of epithelial cells and damaging underlying cells, without the presence of IL-17 at the inflammation site. This could have happened to prevent the development of more severe inflammation, which could lead to the inhibition of colonization. The production of IL-10 is also preventing such inflammations. On the other hand, OMV released by non-pathogenic E. coli appears to influence intestinal homeostasis by causing more anti-inflammatory responses and mild inflammation.
ISSN:1756-0500
1756-0500
DOI:10.1186/s13104-018-3648-3