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Review
. 2020 Nov 7;26(1):101.
doi: 10.1186/s10020-020-00234-7.

The roles of the gut microbiota-miRNA interaction in the host pathophysiology

Affiliations
Review

The roles of the gut microbiota-miRNA interaction in the host pathophysiology

Meihong Li et al. Mol Med. .

Abstract

The gut microbiota regulates the biological processes of organisms acting like 'another' genome, affecting the health and disease of the host. MicroRNAs, as important physiological regulators, have been found to be involved in health and disease. Recently, the gut microbiota has been reported to affect host health by regulating host miRNAs. For example, Fusobacterium nucleatum could aggravate chemoresistance of colorectal cancer by decreasing the expression of miR-18a* and miR-4802. What's more, miRNAs can shape the gut microbiota composition, ultimately affecting the host's physiology and disease. miR-515-5p and miR-1226-5p could promote the growth of Fusobacterium nucleatum (Fn) and Escherichia coli (E.coli), which have been reported to drive colorectal cancer. Here, we will review current findings of the interactions between the gut microbiota and microRNAs and discuss how the gut microbiota-microRNA interactions affect host pathophysiology including intestinal, neurological, cardiovascular, and immune health and diseases.

Keywords: Gut microbiota; Host pathophysiology; miRNA.

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Conflict of interest statement

There is no conflict of interest.

Figures

Fig. 1
Fig. 1
MiRNAs regulate the gut microbiota affecting intestinal homeostasis. a MiRNAs regulate the gut microbiota influencing the intestinal homeostasis of the host. b The mechanism of miR7267-3p alleviating colitis by repressing ycnE expression of the gut microbiota. c MiR-275 protects gut functions in mosquitoes by shaping the gut microbiota. d MiRNAs promote the growth of the gut microbiota through the promotion of transcription, affecting the host CRC. e MiRNA-193a-3p reduces intestinal inflammation by decreasing the uptake of bacterial products. YcnE, monooxygenase ycnE; LGG, Lactobacillus rhamnosus; I3A, indole-3-carboxaldehyde; AHR, aryl hydrocarbon receptor; IL-22, interleukin 22; SERCA, sarco/endoplasmic reticulum Ca2+ adenosine triphosphatase; Fn., Fusobacterium nucleatum; E. coli., Escherichia coli; CRC, colorectal cancer; PepT1, peptide transporter family 1; NF-κB, nuclear factor kappa-B; Pathway diagram key: ┴ inhibition; → induction; ↑ up-regulation; ↓ down-regulation. The figure is referring to the known mechanisms in animal models

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