**2. The gut microbiota in chronic diseases**

The gut microbiota alterations are observed in almost all chronic diseases, including inflammatory bowel diseases (IBD), irritable bowel syndrome, metabolic syndrome, obesity, diabetes, cardiovascular diseases, cancer, neurodegenerative diseases, and mental disorders. Microbiota alterations appear characteristic for each disease state. To date, it is unclear if dysbiosis is a cause or a consequence of the disease [6].

Inflammatory bowel disease is an umbrella term for ulcerative colitis (UC) and Crohn's disease (CD). Changes in the composition of the gut microbiota are reported in patients with IBD, namely a decrease in populations of Firmicutes and Bacteroidetes and an increased Enterobacteriaceae. Other significant differences in gut microbial composition for CD include increased representation by *Ruminococcus gnavus* and decreased beneficial bacteria *Faecalibacterium prausnitzii*, *Bifidobacterium adolescentis*, *Dialister invisus*, as well as an uncharacterized cluster of Clostridium XIVa. IBD patients have a reduced number of butyrate-producing bacteria and an

### *Personalized and Targeted Gut Microbiome Modulation in the Prevention and Treatment… DOI: http://dx.doi.org/10.5772/intechopen.110046*

increased number of sulfate-reducing bacteria, which promote further inflammatory processes [10]. The loss of obligate anaerobes with an increase of facultative anaerobes was also observed in patients with IBD [11]. It has been found that patients with IBD have altered metabolism including defective microbial and intestinal bile acid metabolism [6, 12, 13]. A higher level of fecal trypsin was detected in patients with CD suggesting altered protein degradation [14].

Decreased gut microbial diversity is associated with metabolic syndrome and obesity. The gut microbiota changes in these diseases are characterized by an increased ratio of Firmicutes to Bacteroidetes [15]. It seems that gut microbiota is in close correlation with obesity and can affect the transfer of the number of calories from the diet to the host and the host metabolism of absorbed calories [16].

Type 1 diabetes mellitus (T1D) and type 2 diabetes mellitus (T2D) differ in the mechanisms of pathogenesis. Both types of diabetes are associated with dysbiosis, but with different characteristic patterns. T1D is associated with a decrease in mucin degrading bacteria, *Bifidobacteria*, *Lactobacillus*, and *Prevotella* and an increase in *Bacteroidetes* and *Clostridium.* T2D is characterized by a decrease in *Clostridium* and an increase in *Lactobacillus* and *Bacteroidetes*. In both types of diabetes mellitus, changes of the microbiota were observed such as a decrease in the gut microbiota diversity, a decrease in butyrate-producing bacteria and Firmicutes, disrupted epithelial barrier integrity, and increased gut permeability [12].

Autism spectrum disorders (ASD) are characterized by social and communication deficits and repetitive behaviors. A significant increase in the Firmicutes/ Bacteroidetes ratio was found in autistic individuals due to a decrease in the relative abundance of Bacteroidetes. At the genus level, a decrease in the relative abundance of *Alistipes*, *Bilophila,* and *Parabacteroides* was detected, while *Corynebacterium* and *Lactobacillus* were significantly increased. The increase in Clostridiales bacteria in constipated autistic individuals can be important in the pathogenesis of autism by the production of propionic acid, which can permeate into the brain and cause cognitive impairments [17]. It was also observed that the relative proportion of the fungal genus *Candida* was more than double in autistic than neurotypical subjects, but this difference was only partially significant due to a larger dispersion of values [18].

Dysbiosis in patients with colorectal cancer (CRC) is characterized by a decrease of butyrate-producing bacteria and an increase in the proportion of several potentially pathogenic bacteria. It has been suspected that bacterial species, such as *Bacteroides fragilis*, *Clostridium septicum*, *Fusobacterium spp*., and *Escherichia coli,* are involved in colorectal carcinogenesis. A decrease in Firmicutes and an increase in Proteobacteria, Bacteroidetes, and Fusobacteria were observed in CRC. In colorectal cancer tissue, an increase in the population of *Akkermansia muciniphila* and *Fusobacterium nucleatum* has been detected. It was found that the composition and numbers of dominant microbial species in CRC-associated dysbiosis in the gut lumen differ depending on disease severity and tumor stage [19, 20].
