# Plant-Derived Phytobiotics as Emerging Alternatives to Antibiotics Against Foodborne Pathogens
## 3 Mechanisms of Action of Phytobiotics Against Foodborne Pathogens
### Disruption of Bacterial Cell Wall Integrity, Membrane Structure, and Biofilm Formation  
The first mechanism under discussion involves damage to the bacterial cell membrane by phytobiotics, ultimately leading to cell lysis and death. This mode of action is frequently observed in the case of essential oils and concentrated plant extracts such as thymol,linalool, and menthol. These compounds can disrupt the integrity of the bacterial cell envelope, causing leakage of cellular contents and, consequently, bacterial death [101; 102; 103]. Phytobiotics interfere with bacterial membranes through various mechanisms, beginning with direct membrane damage. Luteolin, for instance, compromises membrane integrity by inducing oxidative stress and cellular damage in _Salmonella enterica_ and _E. coli_[104]. A more specific effect involves the alteration of membrane fluidity. For instance, shikimic acid induces significant leakage of potassium ions and nucleotides from _Staphylococcus aureus_, indicating disruption of membrane integrity and permeability. Furthermore, the study reported changes in membrane potential and a decrease in membrane fluidity [105]. In the same work, [PERSON] and colleagues observed that these mechanisms may overlap, as they also noted interactions with membrane structural components--namely proteins. Cell wall proteins (CWPs) of fungi and yeasts--such as mannoproteins and hydrophobins--are essential for adhesion, pathogenicity, and survival. Phytobiotic interactions with CWPs can disrupt these functions, positioning CWPs as viable targets for antimicrobial strategies. Phytobiotics may interact directly with these proteins or indirectly disrupt their structure, for example, by degrading the polysaccharide scaffold [106]. In Gram-positive bacteria, cell wall proteins are anchored to the peptidoglycan layer via sortase enzymes. Anchored proteins, together with teichoic acids and polysaccharides, play a vital role in bacterial interactions [107]. These structures may serve as molecular targets for phytobiotics. For example, in the study by [PERSON] et al. [108], phytochemical compounds were shown to bind to membrane-associated proteins such as peptide-binding proteins, cell wall surface anchors, pilins, transglycos, and penicillin-binding proteins (PDB IDs: 5079, 7 RJ), 2 XTL, 3 PHS, 3 VMQ, 3 VSK) [108]. In most cases, antimicrobial activity via damage to the bacterial cell wall and membranes is particularly evident with the use of essential oils. For instance, components of essential oils such as citronello1 alter the surface charge and hydrophobicity of bacterial membranes, leading to membrane disruption and potassium leakage [109]. Essential oils are hydrophobic, a property that facilitates their interaction with bacterial cell walls and membranes, ultimately resulting in structural dysfunction [110]. Phytobiotics have also been shown to interfere with or modify lipopolysaccharideaccharides in Gram-negative bacteria and teichoic acids in Gram-positive bacteria, disrupting proper cell wall assembly and increasing bacterial susceptibility to environmental stressors [41; 107]. Induction of oxidative stress by phytobiotics also contributes to antimicrobial activity by destabilizing bacterial cell membranes. This mechanism involves enhanced production of reactive oxygen species (ROS), leading to damage of membrane lipids and proteins, loss of cytoplasmic membrane potential, and disruption of ATP production [111; 112]. Phytobiotics can also cause cytoplasmic content leakage through structural disruption of the cell membrane. Triphenyl sesquineolignans derived from the _Illicium_ genus rupture bacterial membranes, resulting in rapid bactericidal activity [113]. Similarly, isochlorogenic acid C obtained from stevia induces significant leakage of intracellular proteins and potassium ions from _E. coli_, indicating damage to both the inner and outer membranes [114]. Another mechanism involves interference with the synthesis of the bacterial cell wall or membrane.