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Engineered Probiotics for Detection and Treatment of Inflammatory Intestinal Diseases.

ABSTRACT: Inflammatory intestinal diseases such as Crohn's disease and ulcerative colitis have seen an increase in their prevalence in developing countries throughout the current decade. These are caused by a combination of genetic and environmental factors, altered immune response, intestinal epithelium disruption and dysbiosis in the gut microbiome. Current therapies are mainly focused on treating symptoms and are often expensive and ineffective in the long term. Recently, there has been an increase in our understanding of the relevance of the gut microbiome and its impact on human health. Advances in the use of probiotics and synthetic biology have led to the development of intestinal biosensors, bacteria engineered to detect inflammation biomarkers, that work as diagnostic tools. Additionally, live biotherapeutics have been engineered as delivery vehicles to produce treatment in situ avoiding common complications and side effects of current therapies. These genetic constructs often express a therapeutic substance constitutively, but others could be regulated externally by specific substrates, making the production of their treatment more efficient. Additionally, certain probiotics detecting specific biomarkers in situ and responding by generating a therapeutic substance are beginning to be developed. While most studies are still in the laboratory stage, a few modified probiotics have been tested in humans. These advances indicate that live biotherapeutics could have great potential as new treatments for inflammatory intestinal diseases.

SUBMITTER: Barra M

PROVIDER: S-EPMC7137092 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Engineered Probiotics for Detection and Treatment of Inflammatory Intestinal Diseases.

Barra Maria M Danino Tal T Garrido Daniel D

Frontiers in bioengineering and biotechnology 20200331

Inflammatory intestinal diseases such as Crohn's disease and ulcerative colitis have seen an increase in their prevalence in developing countries throughout the current decade. These are caused by a combination of genetic and environmental factors, altered immune response, intestinal epithelium disruption and dysbiosis in the gut microbiome. Current therapies are mainly focused on treating symptoms and are often expensive and ineffective in the long term. Recently, there has been an increase in ...[more]

PMID: 32296696

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Project description:Background:Mononuclear phagocytes, such as monocytes, macrophages, and dendritic cells, are important cellular components of the innate immune system that contribute to the pathogenesis of many intestinal inflammatory diseases. Summary:While mononuclear phagocytes play a key role in the induction of inflammation in many different tissues through production of pro-inflammatory cytokines and chemokines (such as IL-1, TNF, IL-6, IL-8 and MCP-1), free oxygen radicals (also termed 'oxidative burst'), proteases (such as cathepsins) and tissue-degrading enzymes (such as metalloproteinases), resident macrophages as well as dendritic cells in the intestine display an anergic and 'tolerogenic' phenotype mediating tolerance to commensal bacteria. In recent years many single nucleotide polymorphisms (SNPs) in genes mainly expressed in the above-mentioned cell types have been identified to convey an increased risk of autoimmune diseases. SNPs in the NOD2, ATG16L1 and TNFSF15 genes, which are involved in the function of the innate immune cells, are identified as risk factors for Crohn's disease (CD). Of note, these genes are involved in the different functions in the innate immune cells. For example, while NOD2 is required for intracellular recognition of microbial components, ATG16L1 is involved in autophagy responses against intracellular microbes. Likewise, TNFSF15 contributes to the induction of inflammatory responses by innate immune cells. Furthermore, the frequency of mutations in these genes differs by ethnicity. Genetic variations in the NOD2 and ATG16L1 genes are associated with CD in Caucasians but much less in Eastern Asian populations, whereas SNPs in TNFSF15 are dominated in Asian populations. Thus, different genetic risks may eventually lead to similar impairments in innate immune cells, thereby developing the same disease in Western and Asian patients with CD. Key Messages:Despite differences in risk genes, similar mechanisms associated with the innate immune system may trigger autoimmune and chronic inflammatory intestinal diseases in East and West.

Dataset Information

Engineered Probiotics for Detection and Treatment of Inflammatory Intestinal Diseases.

Publications

Engineered Probiotics for Detection and Treatment of Inflammatory Intestinal Diseases.

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