## 3 SRB Impact on Environments and Humans
### Intestinal SRB and Their Association with Diseases  
SRB are a natural part of the colonic microbiota of animals and humans [84; 85; 86; 87; 88; 89]. They are involved in the utilization of H\({}_{2}\) produced in the intestine as a result of the fermentation of sugars. Intestinal SRB use organic compounds as an electron donor [90; 91; 92; 93]. In this respect, they have a competitive relationship with other H\({}_{2}\) metabolizing organisms for the acquisition of electrons, namely methanogenic archaea (for example, _Methanobrevbincter smithii_). The availability of sulfate, which also is a component of food, plays important roles in intestinal SRB growth as well. Endogenous sources of sulfate, such as mucin or chondro sulfate, are also present in the intestine but must be treated by the lytic action of other bacteria such as clostridia [94].  
The defining metabolic by-product associated with SRB is, of course, H\({}_{2}\)S [95; 96; 97]. At higher concentrations, H\({}_{2}\)S has carcinogenic and toxic effects on intestinal cells. It also blocks the binding of oxygen to cytochrome c and inhibits its functionality [98; 99]. By binding to heme \(a\)3 cytochrome, the binding of oxygen is disabled and thereby causes oxidative phosphorylation, interrupting the formation of ATP [99]. H\({}_{2}\)S also acts mutagenically on DNA and, by its ability to reduce disulfide bridges, it can also disrupt protein structures [99; 100; 101; 102; 103]. SRB are often associated with idiopathic intestinal inflammation, such as ulcerative colitis. In this disease, an increased amount of SRB [101] and an increased concentration of H\({}_{2}\)S have been found as compared to healthy patients [102; 103]. However,the results are not showing fully unambiguous correlations. On the other side, the high prevalence of intestinal bowel disease among inhabitants, especially in Western countries, emphasizes the importance of studies dealing with SRB occurrences as well as their intestinal environments [84; 85; 86].  
Bacteria are constantly developing new anti-phage defenses, due to which phages go through constant evolution, too. Anti-phage systems are mainly based on protein components that mediate defense. Protein involvement in anti-phage bacterial systems is the most understood bacterial defense against phages. Chemical anti-phage defense systems are widely developed in _Streptomyces_[104]. Another common bacterial anti-phage system is the microbial cell surface modification that does not allow phage attachment. The CRISPR-Cas defense system represents a more advanced anti-phage bacterial strategy, since it is based on phage sequences, capturing and using it to prime a response that inhibits phage growth. The addition of methyl groups to DNA and degrading other DNA without methyl groups is another bacterial tactic against phages. Certainly, there are also other more specific bacterial single cell developed anti-phage systems and strategies [105].  
Epithelial cells secrete mucin, which creates a chemical and mechanical barrier against bacteria, while also lubricating the intestines and hydrating them. These glycoproteins contain the rigid MUC2 protein. H\({}_{2}\)S degrades the structural integrity of mucous layers by reducing the disulfide bridges that bind mucin units. This causes a decrease in polymer binding, and bacteria can therefore more easily reach the epithelial cells where they can induce an immune response or directly damage the cells [103].