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

• Published in: BMC research notes Vol. 11; no. 1; p. 539
• Main Authors: Behrouzi, Ava, Vaziri, Farzam, Riazi Rad, Farhad, Amanzadeh, Amir, Fateh, Abolfazl, Moshiri, Arfa, Khatami, Shohreh, Siadat, Seyed Davar
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 01.08.2018; BioMed Central; BMC
• 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; United States > US; Germany; Signaling; Outer membrane vesicles; Toll like receptor; Escherichia coli
• ISSN: 1756-0500; 1756-0500
• DOI: 10.1186/s13104-018-3648-3

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.