The Impact of Gut Microbiota on Radiation-Induced Enteritis

Abstract

Radiotherapy is an important treatment for abdominal tumors. A critical side effect for this therapy is enteritis. In this review, we aim to summarize recent findings in radiation enteritis, in particular the role of gut microbiota dysbiosis in the development and therapy of the disease. Gut microbiota dysbiosis plays an important role in the occurrence of various diseases, such as radiation enteritis. Abdominal radiation results in changes in the composition of microbiota and reduces its diversity, which is mainly reflected in the decrease of Lactobacillus spp. and Bifidobacterium spp. and increase of Escherichia coli and Staphylococcus spp. Gut microbiota dysbiosis aggravates radiation enteritis, weakens intestinal epithelial barrier function, and promotes inflammatory factor expression. Pathogenic Escherichia coli induce the rearrangement and redistribution of claudin-1, occludin, and ZO-1 in tight junctions, a critical component in intestinal epithelial barrier. In view of the role that microbiome plays in radiation enteritis, we believe that intestinal flora could be a potential biomarker for the disease. Correction of microbiome by application of probiotics, fecal microbiota transplantation (FMT), and antibiotics could be an effective method for the prevention and treatment of radiation-induced enteritis.

Keywords: inflammatory cytokines; intestinal epithelial barrier; microbiota; probiotics; radiation enteritis.

Figure 1

Microbiota dysbiosis is involved in the development of multiple diseases. The intestinal flora affects immune, metabolism and other functions of the host. Microbiota dysbiosis leads to a series of diseases, such as diabetes and colitis.

Figure 2

Gut microbiota affects the function of intestinal epithelial barrier. Different types of microbiota act on various targets associated with intestinal epithelial barrier. Biffidobactrium, Lactobacilli, Streptococci and Akkermansia muciniphila stimulate the secretion of MUC2. SCFAs produced by Akkermansia muciniphila enter into the intestinal epithelial cells through GPCR to increase the expression of tight junction protein claudin-3 and occludin. Lactobacillus plantarum inhibits pathogenic Escherichia coli growth and increases the expression of ZO-1 and occludin. Biffidobactrium diminishes the formation of LPS and inhibits the TLR-NF-κB signaling to alleviate inflammation, hence decreasing intestinal permeability and bacterial translocation.