## 4 Discussion  
The concept of amendment of bowel microbiota in the pathology of ulcerative colitis (UC) has been generally accepted owing to the confirmation of significant differences in bowel microbiota between healthy individuals and UC patients [27,28]. However, it remains unclear whether the altered bowel microbiota is a cause or a consequence of intestinal inflammation [29]. However, the significant role of microbiota has been confirmed. Dysbiosis is frequently defined as an imbalance within the complex commensal communities associated with a particular disease. The whole-genome studies substantiated significant differences between bowel microbiota in healthy individuals and patients with UC with respect to biodiversity and species richness, which particularly diminish in terms of Firmicutes and Bacteroidetes and show a relative increase in the bacterial species of the Enterobacteriaceae family [27]. In patients suffering from UC, specific signs of bowel microbiota were observed, characterised by an increase in species _Ruminococcus gnaurus_ and a decrease in _Bifidobacterium adolescents, Dialister invisus, Faecalibacterium prausnitzi_, and the species _Clostridium_ cluster XIV [30], and a decrease in genera _Blautia_ and _Roseburia_[31]. In the FMT from the donor used in our study, we detected an abundance of species _Bifidobacterium adolescents_ (22.35%) and _Faecalibacterium prausnitzi_ (4%) and participation of representatives of genera _Roseburia_ and _Blautia_. _Faecalibacterium prausnitzii_, the well-studied important producer of butyrate, is one of the most abundant bacteria in healthy human bowel microbiota, where it amounts to approximately 5% of the total faecal microbiota [32]. Butyrate plays a critical role in preventing the development of UC by promoting the regeneration of colonocytes and maintaining intestinal integrity [33]. In addition, butyrate also induces development of regulatory T cells (Treg) supporting immune tolerance of intestinal mucosa and maintains the balance between Th17 and Treg cells [34]. It was confirmed that the proportion of _F. prausnitzii_ was extremely low in intestinal samples from patients with IBD (inflammatory bowel disease), as well as in those suffering from CD (Crohn's disease) and UC [32]. Based on the ample evidence suggesting its significant replenishment in patients in remission, _F. prausnitzii_ has been proposed as an important diagnostic marker of IBD [35]. In the FMT from the donor used in our study, we also detected the presence of other important producers of butyrate, such as representatives of the species _Coproccus catus_ and _Eubacterium retale_, which also play an important role in the maintenance of health of human intestines. One of the consequences of microbial dysbiosis in patients with UC is the increase in virulent intestinal bacteria of the family Enterobacteriaceae. Bacterial species included in this family comprise a highly endotoxic lipopolysaccharide, the major surface membrane component present in almost all Gram-negative bacteria [36]. Colonisation with Enterobacteriaceae may not itself induce the disease and more likely increases predisposition to the development of intestinal inflammation in IBD [37]. Numerous studies have confirmed a significant increase in enterobacteria, particularly _Escherichia coli_ species, in patients with [PERSON]'s disease (CD) and UC. NGS analysis of FMT from our donor revealed an absence of a major proportion of bacteria of the Enterobacteriaceae family, namely genera _Escherichia_ and _Shigella_. The studies mentioned above substantiate the key role of bowel microbiota in the development of intestinal inflammation, although it still remains unclear whether specific species or bacterial groups may be considered causative agents of UC and CD, or if they only contribute to the aggravation of pathogenesis. The understanding of complex interactions and dynamics within the relevant microbial community could result in the development of a personalised plan of FMT treatment.