**4. Discussion**

Important factors that influence the intestinal environment are sulfate consumption, sulfide production, lactate consumption and acetate accumulation [7–10]. Very often Desulfovibrio genus is present in the intestines and feces of people and animals with inflammatory bowel disease, meaning that this genus plays an important role in the development and occurrence of this ailment. Sulfate is used as a terminal electron acceptor by these bacteria, the same as organic compounds are used as electron donors in their metabolism [6,7]. Leading us to the conclusion that sulfate in food commodities (some bread, soya flour, dried fruits, brassicas, and sausages, as well as some beers, ciders, and wines) play an important role in the development of bowel disease [13].

The principal component analysis showed that the *Desulfovibrio* strains from individuals with colitis grouped in one cluster by biomass accumulation and sulfide production, while the strains from healthy individuals formed another cluster that included the same parameters. A negative correlation (Pearson correlations, *p* < 0.01) was found between sulfate and lactate consumption. Biomass accumulation and hydrogen sulfide showed lower linear regression (*R*2). The kinetic parameters, biomass accumulation, and sulfide production have an important role in bowel inflammation, including ulcerative colitis. Acetate produced by SRB probably has a synergy interaction with H2S since sulfate consumption and lactate oxidation represent minor factors in bowel disease [16].

Optimum growing conditions for the bacteria were provided by the study. The intensive growth of *D. piger* Vib-7 was observed in the presence of higher electron acceptor and donor concentrations. Consequently, the intensive accumulation of sulfide and acetate occurs too. According to previous studies and literature data, these conditions are the probable cause of ulcerative colitis, leading to bowel cancer. Hydrogen sulfide negatively a ffects intestinal mucosa, epithelial cells, the growth of colonocytes [4,14–18,36–39], causes phagocytosis, causes the death of intestinal bacteria [4,12,24], and induces hyperproliferation and metabolic abnormalities of epithelial cells [12]. The presence of SRB and high level of metabolites are also connected with colon inflammation [4,6,38]. Hydrogen sulfide concentrations are regulating the integrity of colonocytes [37–39]. In the samples of individuals with ulcerative colitis was also found that SRB sulfide production is higher [5,6]. According to another study dealing with the SRB metabolic process was found that the strains isolated from people with colitis shifted to the right side of the Y-axis by biomass accumulation, sulfate consumption, lactate oxidation, same as hydrogen sulfide and acetate production, in comparison with the strains isolated from healthy individuals. The percentages were di fferences observed in shifting to the right side of the Y-axis: biomass accumulation 26%, sulfate consumption 1.5%, and sulfide production 5% [14]. The intestinal microbiota is a complex system, interactions occur between clostridia, methanogens, lactic acid bacteria, etc. Though, SRB plays a central role in the development of IBD, including ulcerative colitis [1–3,11]. Lactic acid bacteria, methanogens, and many other intestinal microorganisms can be inhibited by hydrogen sulfide produced by SRB [2].

Preservatives added to food often contain sulfur oxides, sulfate polysaccharides (mucin), chondroitin sulfate, carrageenan, and other food commodities represent the source of sulfate and lead to evaluated sulfate intake in the daily diet that leads to increase of hydrogen sulfide concentrations produced by SRB. The western diet contains over 16.6 mmol sulfate/day [13] and the feces of about 50% of healthy individuals contain SRB (*Desulfovibrio*: up to 92%) [1,5,24]. On the other hand, the concentrations of hydrogen sulfide are toxic not only for the intestinal environment but also for their producers. The concentrations higher than 6 mM stop the growth of *Desulfovibrio*, but metabolic activity was not 100% inhibited (the results supported by cross-correlation and principal component analysis). 5 mM concentrations of H2S resulted in two times and eight times longer lag phase and generation time, respectively [18]. It should be noted that clostridia can also produce hydrogen sulfide, but in smaller quantities and can be interacted with SRB [40] Terminal oxidative processes in the large intestine of humans can be also included in the activities of SRB. The connections between SRB presence and activity in the intestine and occurrence of ulcerative colitis were also found in animal studies where SRB isolated from mice with UC produced 1.14 times (higher hydrogen sulfide production rate can damage aggressively intestinal mucosa) more sulfide ions than SRB isolates from healthy mice [6].

It is of crucial importance that all issues concerning H2S metabolic processes and its influence on the gastrointestinal environment are well studied and tested. Since it has been observed in animal studies that H2S-releasing agents can be seen as promising therapeutic agents for many indications [41]. H2S is confirmed to represent an important signaling factor for cardiovascular and nervous systems statute [42]. The way how cecal musoca protects itself from the toxical e ffects of H2S is the conversion to thiosulfate. Consequently, these metabolic pathways play an important role in the occurrence of ulcerative colitis [43]. The importance of similar studies can be seen through the fact that mechanisms leading to Chron's disease still remain unclear [44].

According to meta-analysis, SRB occurs more often in patients with UC. The finding can be explained by the fact that counts of SRB are lower (though still detectable) in healthy individuals. Oppositely, in patients with developed inflammatory bowel disease, the production of H2S reaches toxic levels and also destroyed its producers (sulfate-reducing bacteria) [15].
