## 4 Discussion
This condition is negative because the SCFA strengthen the intestinal barrier and the immune system in the defense against pathogens. At the same time, levels of harmful microorganisms rise; these include bacteria, mostly Gram-negative bacteria, that lysing lipopolysaccharideackage (LPS) in the gut lumen facilitate its entry into bloodstream and may lead to a deleterious pro-inflammatory systemic immune response [32]. It is also known that dysbiosis leads to an increase of bacterial populations that stimulate tumorigenesis and contribute to epithelial carcinogenesis and tumor progression by altering metabolic properties (such as bile acid and butyric acid) and inflammatory process. In many human intestinal diseases, such as [PERSON]'s disease and ulcerative colitis, significant changes in gut microbiota have been reported [33; 34; 35]. In these pathological conditions, as well in CRC patients [4], again, one of the major biological effects observed is a reduction/substitution of butyrate-producing bacteria. Butyrate, one of the SCFAs, is a major metabolite in colonic lumen arising from bacterial fermentation of dietary fiber and has been shown to be a critical mediator of the colonic inflammatory response. Butyrate has been implicated in the protection against colitis and CRC by reducing oxidative damage to DNA, inducing apoptosis in DNA-damaged cells, inhibiting tumor cell growth, and decreasing the activity of co-carcinogenic enzymes [36; 37]. Butyrate possesses both preventive and therapeutic potential to counteract inflammation-mediated ulcerative colitis (UC) and colorectal cancer. Emerging data suggest that certain groups of bacteria might promote whereas others might protect against colon cancer. Indeed, _Fusobacterium nucleatum_ seems to play a central role in the tumor microenvironment as its abundance correlates with cancer progression as well as the dysbiosis tumor microbiota composition including _Bacteroides_ spp, the enterotoxigenic _Bacteroides fragilis_ in particular, and _Prevotella_ species, may also promote colorectal cancer by stimulating exaggerated immune responses via Th17 cells [38]. [PERSON] and coworkers reported an increase of acetic and butyric acids in colon contents of pigs, when a commercially available probiotic strain _Pediococcus pentosaceus_ was administrated [39], a Gram+ coccus again present only in fecal samples of control subjects. Concerning the greater presence of _Bacteroides vulgatus_ and _Bacteroides uniformis_ in control stool samples compared to SCA/P subjects, it is worth mentioning the findings by [PERSON], which studied the discrepancies of gut microbiota between healthy subjects and CRC patients, reporting a structural segregation between the two populations [4]. In his report, [PERSON] identified forty-eight operational taxonomic units (OTUs) by redundancy analysis as key variables significantly associated with the structural difference. One OTU closely related to _Bacteroides fragilis_ (98.1% similarity) was enriched in the gut microbiota of CRC patients, whereas two OTUs related to _Bacteroides vulgatus_ (100% and 98.7% similarity, respectively) and one to _Bacteroides uniformis_ (97.5% similarity) was enriched in that of healthy volunteers. Revisiting our data, it is clear that _Bacteroides fragilis_ is present only in the fecal samples of the SCA/P subjects, while _Bacteroides vulgatus_ and _Bacteroides uniformis_ are predominant in the feces of control subjects confirming, in part, the data coming from [PERSON]'s report [4]. Several authors suggest that an altered composition in the gut microbiota, including the loss of microbiota diversity (LOMD), determines a predisposing microenvironment for dysbiosis. LOMD appears as a common feature of most dysbiosis and it is a constant finding of intestinal dysbiosis [40]. In digestive diseases such as [PERSON]'s disease [41; 42], irritable bowel syndrome, with [43] or without diarrhea [44] and colorectal cancer [45], LOMD is constantly observed.