Exploring interplay between bovine milk-derived α-lactalbumin, pathogenic bacteria, and bacteriophages at the...

There is so far no available data about how the additive, synergistic, or antagonistic effects of the combined form of alpha-lactalbumin (α-La) and bacteriophages might modulate the cellular milieu of the host-pathogen interface. A co-culture of colonocytes and hepatocytes was stimulated with Pseudomonas aeruginosa PAO1 in the presence of KPP22 phage and incubated for 6 hours in medium alone or medium supplemented with bovine milk-origin α-La. The combination of KPP22 phage and α-La significantly inhibited P.a PAO1-elicited secretion of IL-1β, IL-6, and ICAM-1, which are the mediators and enzymes associated with the inflammatory response to an infectious-inflamed milieu. Cell viability was higher in the P.a PAO1+ KPP22 phage group compared to the P.a PAO1alone group. KPP22 phage and α-La, either alone or in combination, rescued P.a PAO1-induced aberrant PGE1/PGE2 production ratios. The convergence of ingested α-La and phages mitigates pro-inflammatory mediators. α-La leads to an increased sensitivity of opportunistic pathogenic bacteria to phages. Structural, functional, or immunological similarities between ingested α-La and phages play an important role in the mitigation of infection-driven pathobiological processes.