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Article 13, 4/2016


Microbiota Small RNAs in Inflammatory Bowel Disease

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Anca T. Filip1, Ovidiu Balacescu2, Catalin Marian1, Andrei Anghel1

1) Biochemistry Department, Victor Babes University of Medicine and Pharmacy, Timisoara;
2) Department of Functional Genomics, Proteomics and Experimental Pathology, Prof. Dr. I. Chiricuta Oncology Institute, Cluj-Napoca, Romania

DOI: http://dx.doi.org/10.15403/jgld.2014.1121.254.lip

MiRNAs are a class of potential gene regulators of critical importance in Inflammatory Bowel Disease (IBD). This review aims to present the connection between gut microbiota, probiotics administration and microRNA (miRNA) expression in IBD. It also brings into question cross-kingdom RNAi (RNA interference). Not only that gut host cells garden the intestinal microbiome via miRNA, but also strong evidence supports the idea that different species of bacteria have an impact on the intestinal immune response by modulating miRNA expression. Cross-kingdom RNAi refers to RNA silencing signals that travel between two unrelated, interacting organisms. RNAs communication between prokaryotes and eukaryotes (bacteria and nematodes) via RNAs transfer has been proved. Some authors also support the idea that non-coding RNAs are being transferred by bacterial pathogens to the host cells as part of the intracellular infection process. Further studies are required in order to clarify whether the mechanism by which bacteria modulate miRNA expression concerns RNAs transfer. These findings may lead to a different approach to IBD therapy in the future.

Key words: bacteria – gastrointestinal microbiome – microRNAs – probiotics – RNA interference.

Abbreviations: AChE: Acetylcholinesterase; AIEC: Adherent-invasive E coli; ATF: Activating transcription factor; Bcl-2: B-cell lymphoma 2; BMDC: Bone marrow-derived dendritic cells; C elegans: Caenorhabditis elegans; CCL: Chemokine C-C motif ligand; CD: Crohn’s disease; CDC42: Cell division control protein 42 homolog; CXCL: Chemokine (C-X-C motif) ligand; DC: Dendritic cells; E Coli: Escherichia coli; EcN: E coli Nissle; EPEC: Entheropathogenic E coli; FOXO3: Forkhead box protein O3; GF: Germ-free; IBD: Inflammatory bowel disease; IECs: Intestinal epithelial cells; IGLC: Immunoglobulin Lambda Constant Region; IkB: Inhibitor of NF-Kb; IL: Interleukin; IRGM: Immunity-related GTPase family M protein; L del: Lactobacillus delbrueckii; LGG: Lactobacillus rhamnosus GG; MAPK: Mitogen-activated protein kinases; miRNA: MicroRNA; mRNA: Messenger RNA; MyD88: Myeloid differentiation primary response gene 88; NF-kB: Nuclear factor kappa B; NOD2: Nucleotide-binding oligomerization domain-containing protein 2; PAR: Partitioning defective protein; RhoB: Ras Homolog Family Member B; RISC: RNA induced silencing complex; RNAi: RNA interference; SHH: Sonic hedgehog (gene); SPF: Specific-pathogen-free; SRNA: Small RNA; STAT3: Signal transducer and activator of transcription 3; TGF: Transforming growth factor; Th17: T helper 17 cells; TJ: Tight junction; TLR: Toll like receptor; TNF: Tumor necrosis factor; UC: Ulcerative colitis; Xcv: Xanthomonas campestris pv. Vesicatoria; ZO-2: Zonula occludens-2.