Effects of probiotics and prebiotics on intestinal microbiota in mice with acute colitis based on 16S rRNA gene sequencing

Abstract

BackgroundImbalance of intestinal microbiota was closely related to colitis. Under these circumstances, regulation of enteric flora may be beneficial to the repair of inflammation. We aimed to investigate the effects of probiotics (Bifidobacterium and Lactobacillus), prebiotics and their combination on inflammation, and microflora in mice of acute colitis.MethodsC57BL/6J mice were divided into six groups randomly (blank control group, model control group, probiotics group, synbiotics group, lactitol group and probiotics + lactitol group). Each group was given 2.5% dextran sulfate sodium drinking water for 5 days other than the blank control group. Except for the model control group, the other four groups were intervened with probiotics, synbiotics (probiotics and inulin), lactitol, and probiotics + lactitol. Mice were sacrificed after 1 week of gavage, and pathologic scores were calculated. The feces of different periods and intestinal mucosa samples were collected to analyze the differences of intestinal microbiota by 16S rRNA sequencing. Differences of two groups or multiple groups were statistically examined through unpaired Student t test and analysis of variance (ANOVA), respectively. ANOVA, Tukey, Anosim, and metastats analysis were used to compare differences of microbiota among different groups.ResultsAfter gavage for 1 week, the pathologic scores of groups with the intervention were significantly lower than those in the model control group, and the difference was statistically significant (P < 0.05). The model control group was higher in the genus of Bacteroides (relative abundance: 0.3679 vs. 0.0099, P = 0.0016) and lower in Lactobacillus (relative abundance: 0.0020 vs. 0.0122, P = 0.0188), Roseburia (relative abundance: 0.0004 vs. 0.0109, P = 0.0157), compared with the blank control group. However, the same phenomenon was not found in groups gavaged with probiotics and lactitol. Compared with model control group, mice with intervention were increased with Bifidobacterium (relative abundance: 0.0172 vs. 0.0039, P = 0.0139), Lachnospiraceae_NK4A136_group (relative abundance: 0.1139 vs. 0.0320, P = 0.0344), Lachnospiraceae_UCG-006 (relative abundance: 0.0432 vs. 0.0054, P = 0.0454), and decreased with Alistipes (relative abundance: 0.0036 vs. 0.0105, P = 0.0207) in varying degrees. The mucosal flora was more abundant than the fecal flora, and genus of Mucispirillum (relative abundance: 0.0207 vs. 0.0001, P = 0.0034) was more common in the mucosa. Lactitol group showed higher level of Akkermansia than model control group (relative abundance: 0.0138 vs. 0.0055, P = 0.0415), probiotics group (relative abundance: 0.0138 vs. 0.0022, P = 0.0041), and synbiotics group (relative abundance: 0.0138 vs. 0.0011, P = 0.0034), while probiotics + lactitol group had more abundant Akkermansia than synbiotics group (relative abundance: 0.0215 vs. 0.0013, P = 0.0315).ConclusionsProbiotics and prebiotics reduce the degree of inflammation in acute colitis mice obviously. Mice with acute colitis show reduced beneficial ...

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“…It is worth highlighting this work, since Akkermansia seems to ameliorate the inflammatory response and insulin resistance in obese and diabetic patients [72], protecting the intestinal epithelial cells and enhancing the mucosal barrier function [73]. As the genome of Akkermansia was proved to be able to encode a wide variety of secretory proteins such as glycohydrolyzases [74], the authors speculated that Akkermansia might be able to decompose lactitol and promote its own proliferation [75]. Furthermore, the supplementation of probiotics and prebiotics, including lactitol, induced an increment of the proportion of helpful bacteria and regulated the balance of the intestinal microbiota [75].…”

“…As the genome of Akkermansia was proved to be able to encode a wide variety of secretory proteins such as glycohydrolyzases [74], the authors speculated that Akkermansia might be able to decompose lactitol and promote its own proliferation [75]. Furthermore, the supplementation of probiotics and prebiotics, including lactitol, induced an increment of the proportion of helpful bacteria and regulated the balance of the intestinal microbiota [75]. For instance, the abundance of Bifidobacterium was increased in all the experimental groups in comparison with the control.…”

“…For instance, the abundance of Bifidobacterium was increased in all the experimental groups in comparison with the control. However, the observed effect might not be exerted by lactitol itself [75]. Another study was performed in Korean adults to evaluate the efficacy of supplementation with the prebiotic UG1601 (based on inulin (61.5%), lactitol (34.6%), and an aloe vera gel (3.9%)) for 4 weeks to alleviate the symptoms of constipation associated with the gut microbiota [70].…”

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“…in the intestinal microbes of mice with acute colitis is significantly lower than that of the mice in the blank control group ( P =0.0139), and the relative abundance of Lachnospiraceae_NK4A136_group spp. in mice after interventions with prebiotics and probiotics is significantly higher than that in model mice ( P =0.0344) [ 42 ]. Members of the Lachnospiraceae family are involved in maintaining colon health and produce butyric acid to prevent colon cancer in humans [ 43 ].…”

Effects of Probiotics <i>Lactobacillus reuteri</i> and <i>Clostridium butyricum</i> on the Expression of Toll-like Receptors, Pro- and Anti-inflammatory Cytokines, and Antimicrobial Peptides in Broiler Chick Intestine

“…In chicken, mice, and piglets, live probiotics have been suggested to induce dynamic changes in the microbiome, and a factor regulating them may be the short-chain fatty acids in the intestinal contents ( Wang et al , 2019 ; Vemuri et al , 2019 ; Neijat et al , 2019 ; Cao et al , 2019 ). Additionally, butyrate has been reported to enhance not only epithelial cell proliferation with the development of villi ( Guilloteau et al , 2010 ; Ahsan et al , 2016 ) but also the mucosal barrier by tight junctions ( Peng et al , 2009 ; Guilloteau et al , 2010 ) and induction of host defense peptide expression including AvBDs and CATHs in the chick intestine ( Peng et al , 2009 ; Sunkara et al , 2011 , 2014 ).…”