Colonisation of the nasopharynx by Streptococcus pneumoniae (the pneumococcus) precedes infection and disease. Mounting evidence suggests that probiotic bacteria could play a role in reducing the risk of respiratory tract infections. We previously demonstrated that the probiotic Streptococcus salivarius inhibits pneumococcal adherence to epithelial cells in vitro.
This study investigates the mechanism of inhibition, including the role of megaplasmid-encoded bacteriocins (antibacterial peptides). Several S. salivarius strains (K12, M18) harbouring megaplasmids (encoding several bacteriocins), and their megaplasmid-negative derivatives, were tested for the ability to inhibit pneumococcal growth on solid media, and their adherence to human pharyngeal epithelial cells (Detroit 562). Pneumococcal adherence was compared following 1) pre-administration of S. salivarius, 2) pre-administration followed by removal of non-adherent S. salivarius, and 3) pre-administration of S. salivarius into permeable transwell inserts.
Only megaplasmid-positive S. salivarius inhibited pneumococcal growth on solid media. However, both megaplasmid-positive and -negative strains of S. salivarius inhibited pneumococcal adherence. Inhibition was unaffected by removal of unbound S. salivarius following pre-administration. No inhibition was observed in preliminary transwell experiments.
Our results suggest that inhibition of pneumococcal adherence mediated by S. salivarius K12 does not require the bacteriocin-encoding megaplasmid, but does require contact of S. salivarius K12 with host cells. As such, inhibition of pneumococcal adherence seems likely to be mediated by competition for binding, rather than by megaplasmid-encoded bacteriocins. This work may facilitate the development of novel strategies for the prevention of pneumococcal colonisation and disease.