BackgroundFecal microbiota transplantation (FMT) is a microbiota-based therapy that shows therapeutic potential in recurrent or refractory Clostridium difficile infections and other intestinal or extra-intestinal disorders. Nonetheless, adverse events (AEs) remain a major challenge in the application of FMT.AimTo review the AEs of FMT and to address the concerns of safety during the procedure.MethodsPublications were retrieved in the databases of Medline, Embase and Cochrane Library. AEs were classified according to their causality with FMT or their severity.ResultsA total of 7562 original articles about FMT were identified in this study, 50 of them fulfilled the inclusion criteria. Totally 78 kinds of AEs were revealed enrolled in these 50 selected publications. The total incidence rate of AEs was 28.5%. Among the 42 publications, 5 kinds were definitely and 38 kinds were probably related to FMT. The commonest FMT-attributable AE was abdominal discomfort, which was reported in 19 publications. For upper gastrointestinal routes of FMT, 43.6% (89/204) patients were compromised by FMT-attributable AE, while the incidence dropped to 17.7% (76/430) for lower gastrointestinal routes. In contrast, the incidences of serious adverse events (SAEs) were 2.0% (4/196) and 6.1% (40/659) for upper and lower gastrointestinal routes, respectively. A total of 44 kinds of SAEs occurred in 9.2% patients, including death (3.5%, 38/1089), infection (2.5%, 27/1089), relapse of inflammatory bowel diseases (0.6%, 7/1089) and Clostridium difficile infection (0.9%, 10/1089).ConclusionConsequently, both AEs and SAEs are not rare and should be carefully monitored throughout FMT. However, high quality randomized controlled trials are still needed for the more definite incidence of AEs of FMT.

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New evidence has emerged in recent years to suggest a strong link between the human gut microbiota, its metabolites, and various physiological aspects of hosts along with important pathophysiological dimensions of diseases. The research indicates that the gut microbiota can facilitate metabolite production in two ways: first, the resident species of the gut microbiota use the amino acids produced from food or the host as elements for protein synthesis, and second, conversion or fermentation are used to drive nutrient metabolism. Additionally, the gut microbiota can synthesize several nutritionally essential amino acids de novo, which is a potential regulatory factor in amino acid homeostasis. The primary objective of this review is to summarize the current literature relating to the ways in which microbial amino acids contribute to host amino acid homeostasis.

Disturbed balance between microbiota, epithelial cells, and resident immune cells within the intestine contributes to inflammatory bowel disease (IBD) pathogenesis. The Citrobacter rodentium -induced colitis mouse model has been well documented. This model allows the analysis of host responses to enteric bacteria and facilitates improved understanding of the potential mechanisms of IBD pathogenesis. The current study evaluated the effects of dietary 30 mg/kg quercetin supplementation on C. rodentium -induced experimental colitis in C57BL/6 mice. Following dietary quercetin supplementation, the mice were infected with 5 × 10 8 CFU C. rodentium , and the pathological effects of C. rodentium were measured. The results showed that quercetin alleviated the effects of C. rodentium -induced colitis, suppressed the production of pro-inflammatory cytokines, such as interleukin (IL)-17, tumor necrosis factor alpha, and IL-6 ( p < 0.05), and promoted the production of IL-10 in the colon tissues ( p < 0.05). Quercetin supplementation also enhanced the populations of Bacteroides , Bifidobacterium , Lactobacillus, and Clostridia and significantly reduced those of Fusobacterium and Enterococcus ( p < 0.05). These findings indicate that dietary quercetin exerts therapeutic effects on C. rodentium -induced colitis, probably due to quercetin’s ability to suppress pro-inflammatory cytokines and/or modify gut microbiota. Thus, these results suggest that quercetin supplementation is effective in controlling C. rodentium -induced inflammation.

The pathogenesis of inflammatory bowel disease (IBD) is linked to an intricate association of environmental, microbial, and host-related factors. This study examined the potential effects of dietary addition of two preparations from onion, one comprising quercetin aglycone alone (Q: 0.15% polyphenols, quercetin aglycone:quercetin monoglycosides, 98:2) and another comprising quercetin aglycone with monoglycosides (Q+MQ: 0.15% total polyphenols, quercetin aglycone:quercetin monoglycosides, 69:31), on dextran sodium sulphate- (DSS-) induced colitis in mice. The results revealed a significant decrease in the body weight gain of the mice with DSS-induced colitis, which was counteracted by the dietary Q or Q+MQ supplementation. Meanwhile, the oxidative stress indicated by myeloperoxidase (MPO), reduced glutathione (GSH), malondialdehyde (MDA), and serum nitrate (NO) concentrations was higher in mice with DSS-induced colitis than in the control group mice, but dietary Q or Q+MQ supplementation counteracted this trend. The colitis mice demonstrated reduced Chao1, angiotensin-converting enzyme (ACE), and Shannon indices and an increased Simpson index, but the colitis mice receiving dietary Q or Q+MQ exhibited higher Chao1, ACE, and Shannon indices and a reduced Simpson index. In conclusion, this research showed that even at a low dose, dietary Q or Q+MQ supplementation counteracts DSS-induced colitis in mice, indicating that Q or Q+MQ may be used as an adjuvant therapy for IBD patients.