10 research outputs found

    The role of microbiota and immune system crosstalk in cancer development and therapy

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    Cancer is a multifactorial disease that is the second leading cause of death after cardiovascular disease in the world. In recent years, microbiota's role in the regulation and homeostasis of the immune system has been considered. Moreover, the immune system can affect the microbiota content. These interactions are critical to the functioning of the immune system. Numerous studies in animal and human models have shown the association of changes in microbiota components with the formation of an inhibitory microenvironment in the tumor and its escape from the immune system. Microbiota also plays a crucial role in the success of various anti-tumor treatments, and its modification leads to success in cancer treatment. The success of anti-tumor therapies that directly target the immune system, such as immune checkpoint blockade and T cell therapy, is also affected by the patient's microbiota composition. It seems that in addition to examining the patient's genetics, precision medicine should pay attention to the patient's microbiota in choosing the appropriate treatment method, and together with usual anti-tumor therapies, microbiota may be modified. This review discusses various aspects of the relationship between microbiota and anti-tumor immunity and its successful treatment

    Introduce a novel post-biotic against Pseudomonas aeruginosa biofilm formation using Escherchia coli Nissle1917 outer membrane vesicles

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    Abstract Pseudomonas aeruginosa is an opportunistic bacterial pathogen that can cause acute infections as well as chronic ones in humans. The expression of algD and PpyR genes involved in biofilm formation in clinical isolates of P. aeruginosa in the presence of Escherichia coli Nissle1917 outer membranes vesicles (EcN OMVs) was evaluated. All isolates were tested for biofilm formation. qPCR and disk diffusion were used to identify the expression of algD and PpyR genes, and antimicrobial resistance, respectively. EcN OMVs caused a more significant loss of algD and PpyR expression, compared with the control group. EcN OMVs contain a variety of biomolecules that are capable of influencing the biofilm formation genes. EcN OMVs treatment reduced P. aeruginosa biofilm formation significantly, which emphasizes their positive role in inhibiting biofilm formation. As a result, EcN OMVs can be used as new therapeutic strategies for inhibiting P. aeruginosa biofilm formation

    Impact of gut microbiota on immune system

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    The commensal microflora collection known as microbiota has an essential role in maintaining the host's physiological homeostasis. The microbiota has a vital role in induction and regulation of local and systemic immune responses. On the other hand, the immune system involves maintaining microbiota compositions. Optimal microbiota-immune system cross-talk is essential for protective responses to pathogens and immune tolerance to self and harmless environmental antigens. Any change in this symbiotic relationship may cause susceptibility to diseases. The association of various cancers and autoimmune diseases with microbiota has been proven. Here we review the interaction of immune responses to gut microbiota, focusing on innate and adaptive immune system and disease susceptibility

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

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    Abstract Objective 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. Results 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

    MOESM2 of Comparative study of pathogenic and non-pathogenic Escherichia coli outer membrane vesicles and prediction of host-interactions with TLR signaling pathways

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    Additional file 2. Clustergram plot of genes involved in TLRs signalling pathways. In order to demonstrate a heat map dendrograms, showing the co-regulated genes, a clustergram for the entire dataset was mapped, using non-supervised hierarchical clustering

    MOESM1 of Comparative study of pathogenic and non-pathogenic Escherichia coli outer membrane vesicles and prediction of host-interactions with TLR signaling pathways

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    Additional file 1. Expression analysis of TLRs and interleukins in Caco2 stimulation. Caco2 after 24 h stimulation with OMVs. Data are presented as fold-change compared to untreated control cells. Statistical differences were assessed by the t-test. ∗ p ≤ 0.05, versus control cells
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