miR-301, pleiotropic MicroRnA in Regulation of inflammatory Bowel Disease and ColitisAssociated Cancer
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Date
2018Author
Somesh Baranwal
Rawat, Shiv Govind
Gupta, Pooja
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Inflammatory bowel disease (IBD) is a chronic idiopathic, relapsing, and remitting immune disorders of gastrointestinal tract which consist of two forms, i.e., Crohn’s disease (affect the whole gastrointestinal tract) and ulcerative colitis (restrict to colon only). Recent data demonstrate that IBD arises from the complex interplay of genetic and environmental factor caused by a change in the intestinal microbiota (1). Innate immunity in gastrointestinal system includes epithelial cell layers that express tight cell–cell contact, secreted mucous layer which prevent entry of microbes, protective plasma protein, and circulating leukocytes, such as phagocytic macrophages, neutrophils, dendritic cells (DC), natural killer (NK) cells, NK T-cell, and innate lymphoid cells. The innate immune response also includes complement proteins, defensins, and chemokines which attract inflammatory leukocytes, lipid mediator of inflammation, bioactive amines, and enzymes to enhance inflammation (2). Following exposure to pathogens, the innate immune cells of gastrointestinal mucosa release pro-inflammatory cytokines and activate an adaptive immune response to aggravating inflammation in the intestine (3). Single layered intestinal epithelial cells (IECs) establish a semipermeable intestinal barrier (IB) which allows the dual role of transporting nutrients and avoiding the passage of pathogens. Selective permeability of IECs is achieved by apical junctional complex (AJC) proteins which comprise tight junctions, adherens junctions, and desmosomes to maintain the apicobasal cell polarity and intestinal tissue integrity (4). Dysregulation in intestinal epithelial monolayer cause abnormal interaction with immune cells and perturb the intestinal immune homeostasis which is associated with the clinical symptoms of IBD. Studies in the past decade have demonstrated the essential roles of several AJC protein, including underlying actinomyosin components, actin isoforms, and intracellular signal transducer and activator of transcription (STAT) transcription factors, and nuclear factor-κB (NF-κB) in the maintenance and remission of IBD progression (5).
Journal
Frontiers in Immunology