Abstract
Streptococcus pyogenes [Group A streptococcus (GAS)], a frequent colonizer of the respiratory tract mucosal surface, causes a variety of human diseases, ranging from pharyngitis to the life-threatening streptococcal toxic shock-like syndrome. Lactobacilli have been demonstrated to colonize the respiratory tract. In this study, we investigated the interference of lactobacilli with the virulence phenotypes of GAS. The Lactobacillus strains L. rhamnosus Kx151A1 and L. reuteri PTA-5289, but not L. salivarius LMG9477, inhibited the hemolytic activity of S. pyogenes S165. The inhibition of hemolytic activity was attributed to a decrease in the production of streptolysin S (SLS). Conditioned medium (CM) from the growth of L. rhamnosus Kx151A1 and L. reuteri PTA-5289 was sufficient to down-regulate the expression of the sag operon, encoding SLS. The Lactobacillus strains L. rhamnosus Kx151A1, L. reuteri PTA-5289, and L. salivarius LMG9477 inhibited the initial adherence of GAS to host epithelial cells. Intriguingly, competition with a combination of Lactobacillus species reduced GAS adherence to host cells most efficiently. The data suggest that an effector molecule released from certain Lactobacillus strains attenuates the production of SLS at the transcriptional level and that combinations of Lactobacillus strains may protect the pharyngeal mucosa more efficiently from the initial colonization of GAS. The effector molecules released from Lactobacillus strains affecting the virulence phenotypes of pathogens hold potential in the development of a new generation of therapeutics.
Highlights
A range of bacterial communities including commensals and pathogens colonize the nasopharynx
We investigated the influence of lactobacilli on the hemolytic activity of GAS
This study aimed to investigate how lactobacilli affect the virulence phenotypes of GAS in terms of hemolytic activity and adherence to host epithelial cells
Summary
A range of bacterial communities including commensals and pathogens colonize the nasopharynx. Local pharyngeal infection with GAS manifests as pharyngitis and, if spread from the local site, can cause the systemic diseases sepsis, streptococcal toxic shock syndrome, and necrotizing fasciitis (Luca-Harari et al, 2009). S. pyogenes produces a wide array of virulence factors, enabling it to adhere, invade, and spread within the human host (Cunningham, 2008). The reason why S. pyogenes sometimes causes disease is not entirely understood, but both bacterial virulence factors and host factors are thought to contribute (Cole et al, 2011). Attachment to epithelial cells is the crucial initial step of colonization because non-adherent GAS is removed by mucus and saliva flow. The host responses regulate the bacterial colonization and play a significant role in the pathogenesis of the infection (Ribet and Cossart, 2015)
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