Some of these effects will be driven by a range of genetic and environmental factors (e.g. dispersal patterns and the relative frequency of auto- to allo-infection), while others will be dependent on the population context (e.g. the fitness of competing pathogen races) or be isolate specific (e.g. the extent of fitness costs associated with specific infectivity factors).
Milk oligosaccharides and glycoproteins have demonstrated protective qualities against enteric pathogen infections in infants by enhancing the binding of IgA with pathogens, having an antibacterial activity against pathogens and competing with pathogen binding sites [7], [8], [9].
In addition, by competing with pathogens for nutrients and adhesion in a microbiological niche, probiotics can prevent replication by pathogens, a phenomenon known as colonisation resistance [ 5].
Several methods have been observed: some antagonists produce antibiotics that kill or reduce the number of closely related pathogens; some are parasites on pathogens; and others simply compete with pathogens for available food.
While competing with pathogen for physical occupation of site, BCAs reduce or delay the root colonization by the pathogen.
Bacteriocins can inhibit the invasion of competing or pathogen strains in the community or modulate the composition of the microbiota and the host immune system [ 53].
In both food safety and medicine, the longer the lag phase the longer body defenses have time to fight pathogens, and the longer the natural gut flora have to out-compete the pathogens.
This activity, together with the mechanism of competitive exclusion, in which probiotic strains compete with pathogens for nutrients and attachment sites, would prevent colonization of the intestine by pathogens [ 53].
They have been shown to modulate the permeability of epithelial barriers, alter the inflammatory potential of epithelial cells, compete with pathogens for mucosal colonization, or directly modify the activity of immune cells (reviewed in [10], [11]).
