# Unlocking Wellness: Probiotics as Key Drivers in Functional Food Innovation and Health Promotion
## 3 The Function of Probiotics
### Regulating the Balance of Intestinal Flora  
Intestinal flora balance is critical for intestinal homeostasis. The primary mechanism by which probiotics regulate intestinal balance is through competitive exclusion, a natural phenomenon involving competition for nutrients and adhesion sites [29]. On the one hand, probiotics express adhesins on their surface, which specifically bind to glycoprotein receptors on intestinal epithelial cells, thereby inhibiting the colonization of pathogenic bacteria [30]. On the other hand, probiotics efficiently absorb limited nutrients in the intestine, thereby depriving pathogens of essential resources, competitively inhibiting the growth of harmful bacteria, reducing the production of harmful substances, and maintaining intestinal microbiota balance [31]. [PERSON] et al. [32] evaluated the inhibitory effects of chicken-derived lactic acid bacteria (LAB) on intestinal pathogens, such as _Escherichia coli_ and _Salmonella_ spp. The results showed that _P. pentosacus_ 2-5 and _L. reuteri_ _L-3_ significantly reduced the adherence of pathogenic bacteria to Caco-2 cells in competition, exclusion, and replacement assays, suggesting that they can reduce the colonization of harmful bacteria through competitive inhibition mechanisms. Figure 1: Interrelationships between the effects of probiotics. In addition, probiotics can secrete various metabolic substances with regulatory effects, thereby directly inhibiting the growth of pathogenic bacteria. First, probiotics can secrete bacteriocins, which effectively inhibit the growth of pathogenic bacteria. For example, _Lactococcus lactis_ produces nisin, whose N-terminal domain binds to the pyrophosphate group of the bacterial cell wall precursor (Lipid II), thereby blocking the glycosylation reaction of the peptidoglycan chain and interrupting cell wall synthesis. Simultaneously, Lipid II serves as an anchor to fix nisin to the membrane, allowing its C-terminal amphiphilic helix to insert into the membrane phospholipid layer and flip over. This ultimately leads to the formation of transmembrane pores through the coordinated assembly of multiple molecules, thereby disrupting the integrity of the cell membrane and killing pathogenic bacteria [33]. Probiotics can also directly disrupt the collective cooperation and surface colonization capabilities of pathogenic bacteria by secreting hydrogen peroxide (H\({}_{2}\)O\({}_{2}\)). H\({}_{2}\)O\({}_{2}\) oxidizes quorum sensing (QS) signaling molecules, thereby inactivating them and blocking interbacterial communication, which in turn inhibits the expression of virulence factors. Furthermore, H\({}_{2}\)O\({}_{2}\) oxidizes the conserved cysteine residues in the GGDEF domain of the active center of di-guanosine cyclase, thereby inactivating it and unregulating phosphodiesterase expression, which leads to a sharp decrease in c-di-GMP levels. This both inhibits the expression of extracellular polysaccharide synthesis genes and blocks the mechanism of biofilm formation, thereby effectively inhibiting the biofilm formation ability of pathogenic bacteria [34]. Second, probiotics produce organic acids, which directly lower the intestinal pH, thereby inhibiting the growth and reproduction of pathogenic bacteria. Short-chain fatty acids (SCFAs) play a major role in this process. SCFAs are key metabolic products produced by probiotics through the fermentation of dietary fiber, primarily including acetate, propionate, and butyrate [35]. On one hand, the production of SCFAs significantly lowers the pH of the intestinal contents. On the other hand, acetate and lactate can be directly utilized by beneficial bacteria, such as butyrate-producing bacteria, promoting their growth and metabolic activities. As the population of beneficial bacteria expands, it inhibits the excessive proliferation of pathogens, thereby effectively maintaining microbial balance. Butyrate is a potent histone deacetylase (HDAC) inhibitor.