In humans, a wide number of different microbial species are located in the bowel, which hosts several trillion microbial cells [1]. This ensemble of microbial species is generally called gut microbiota [2]. There is a profound interplay between the gut microbiota and the human biology [3]. Indeed, the gut microbiota is important for various physiological functions such as eliciting immune maturation [4], defending against pathogens colonization and overgrowth [5], influencing epithelial proliferation [6] and intestinal vascular density [7], modifying bile acids in the large bowel [8], promoting metabolic homeostasis [9] and hormone modulation [10], synthesizing vitamins [11] and neurotransmitters [12], supplying energy [1], and regulating bone metabolism [13]. The intestinal microbiota of a healthy subject is composed predominantly by Bacteroidetes and Firmicutes, with also other smaller sections comprised by Actinobacteria, Proteobacteria, Verrucomicrobia, methanogenic archaea, Eucarya, and various phages [1]. Modifications in the constitution and function of gut microbes lead to dysbiosis [1], and several diseases are associated with gut dysbiosis [1,14]. In particular, intestinal dysbiosis is an important feature of inflammatory bowel diseases (IBD) [14,15], playing a crucial role in the onset of the disease in predisposed subjects [16]. Indeed, some important alterations of intestinal microbiota have been identified in IBD, including an underrepresentation of Firmicutes (in particular Faecalibacterium prausnitzii) [17], Bacteroidetes, and Lactobacillus [16] with increased levels of Proteobacteria [18]. IBD are life-long disorders characterized by the chronic relapsing inflammation of the gastrointestinal tract [19,20] with the intermittent need for escalation treatment, eventually requiring surgical intervention [21]. In particular, although decreasing over time, subjects affected by UC still have a 5- and 10-year risk of colectomy of 7.0% and 9.6%, respectively [22]. Indications for colectomy comprise refractory acute severe UC, medically refractory disease, and colorectal cancer [19]. For these cases, restorative total proctocolectomy with ileal pouch–anal anastomosis (IPAA) is the surgical intervention of choice [19,23,24]. Although IPAA provides a good quality of life and satisfactory functional outcomes [25,26], it can be subject to some complications, including pouchitis as the most common [27]. Pouchitis is an active, non-specific, idiopathic inflammation of the IPAA mucosa [28]. Approximately 25% of subjects develop pouchitis a year after IPAA with an increasing trend that reaches up to 45% at 5 years [29]. Approximately 10–20% of the pouchitis may also progress to chronic pouchitis, leading to antibiotic dependency or refractoriness requiring immunosuppressive therapy [30]. Furthermore, pouchitis is a risk factor for hospitalization [31] and pouch failure [32], which can occur in 5–10% of cases [33,34,35]. The etiology of pouchitis is mostly unclear. However, the efficacy of antibiotics in pouchitis suggests that the IPAA-related dysbiosis of the microbiota could play an important role in its pathogenesis [36,37,38]. 

2. IPAA Microbiota Evolution over Time