# Plant-Derived Phytobiotics as Emerging Alternatives to Antibiotics Against Foodborne Pathogens
## 4 Impact of Phytobiotics on Microbiota of Food and the Intestine
### Impact on Gut Microbiota
Garlic also provides other bioactive sulfur compounds such as sulfoxides, disulfides (e.g., diallyl disulfide), and soluble fructans (insulin, fructooligosaccharides) with known prebiotic properties [195]. This unique combination allows garlic to modulate the microbiome through multiple mechanisms. First, allicin and related sulfur compounds inhibit the growth of various intestinal pathogens. Garlic has demonstrated bactericidal effects against _E. coli_, _Salmonella_, _Helicobacter pylori_, _C. perfringens_, _S. aureus_, and _C. albicans_[196,197]. The mechanism involves the reactive -S(O)- groups in these compounds, which interact with bacterial enzymes (e.g., oxidoreductase, proteases), oxidize thiol groups in active sites, and disrupt bacterial metabolism. Second, moderate garlic intake may promote the growth of beneficial bacteria such as _Lactobacillus_ and _Bifidobacterium_, due to its content of fermentable fructans that serve as a carbon source [195]. In vitro experiments have shown that adding powdered garlic to fermentation media increases bifidobacterial counts while simultaneously suppressing the growth of _Clostridium_ and _Enterobacteriaceae_[198]. Furthermore, sulfur metabolites from garlic have been shown to exert anti-inflammatory effects and support the integrity of the intestinal barrier [199]. In animal models, garlic supplementation reduced intestinal permeability, commonly referred to as \"leaky gut\" [200]. All of the aforementioned examples confirm the beneficial effects of phytobiotics on the gut microbiota. Consequently, phytobiotics have been considered as part of dietary interventions aimed at treating, alleviating, or preventing diseases associated with gut dysbiosis. For instance, an anti-inflammatory diet for inflammatory bowel disease was developed and tested in a clinical study involving 40 patients. This diet included, among other things, large amounts of fruits and vegetables, thus providing a rich source of natural phytochemicals while excluding pro-inflammatory foods [201]. Clinical improvement was observed in more than half of the participants, including symptom relief and enhanced quality of life. Although it remains unclear which specific dietary component played the most critical role, it is evident that the phytobiotic-rich diet led to modulation of the gut microbiota. In addition to their antioxidant properties, the anti-inflammatory effects of phytobiotics should also be emphasized in the context of gut microbiota interactions. Curcumin (from turmeric), boswellic acid (from _Boswellia_), quercetin (from onion), rosmarinic acid (from rosmear), berberine (from _Coptis_), catechin (from green tea), and shogaol (from ginger) are all well-documented phytochemicals with established anti-inflammatory activities [202; 203]. When discussing diseases associated with gut dysbiosis, it is also essential to mention colorectal cancer--a major contemporary health concern. Disruptions in the intestinal microbial consortium, or the presence of an aberrant microbiota, may contribute to carcinogenesis among various other factors [204]. Many phytochemicals exhibit both anticancer and anti-inflammatory effects on colorectal cancer cells [205]. Notably, these same plant-derived compounds also influence gut microbial ecology, and such changes can occur rapidly--within just a few days of adopting a phytochemical-rich diet [206]. Similarly, polyphenol-rich extracts from sources such as green tea, honey, paprika, blackcurrant, raspberry, cinnamon, and peppermint have demonstrated inhibitory effects against _H. pylori_--a bacterium linked not only to gastric ulcers but also to an elevated risk of colorectal cancer [207]. Phytobiotics exert their effects by modulating key inflammatory signaling pathways such as NF-kB, MAPK, STAT, and Nrf2--central regulators of the host inflammatory response. These compounds reduce the production of pro-inflammatory cytokines (e.g., interleukins, TNF-\(\alpha\)) and mediators such as nitric oxide and prostaglandin E2, thereby suppressing inflammation [203; 208; 209].