Lactobacilli require physical contact to reduce staphylococcal TSST-1 secretion and vaginal epithelial inflammatory response

Staphylococcus aureus biofilms can be found on vaginal epithelia, secreting toxins and causing inflammation. The co-vaginal species Lactobacillus can alter staphylococcal-induced epithelial secretion of inflammatory cytokines and quench staphylococcal toxic shock syndrome toxin-1 secretion. It is hypothesized that these effects of lactobacilli require direct physical contact between lactobacilli, staphylococci and the epithelium. Indeed, lactobacilli only reduced S. aureus-induced inflammatory cytokine expression when allowed physical contact with vaginal epithelial cells. Furthermore, a reduction in toxic shock syndrome toxin-1 secretion only occurred when a probiotic Lactobacillus strain was allowed contact, but not when being physically separated from S. aureus. Bacterial-probe atomic force microscopy demonstrated that lactobacilli and staphylococci strongly adhere to epithelial cells, while lactobacilli adhere stronger to staphylococci than staphylococci to each other, giving lactobacilli opportunity to penetrate and reside in staphylococcal biofilms, as visualized using confocal laser scanning microscopy with fluorescence in situ hybridization probes. These results identify that physical contact and biochemical signaling by lactobacilli are intrinsically linked mechanisms that reduce virulence of S. aureus biofilm. Lactobacilli need physical contact with pathogens and vaginal epithelia to reduce toxin secretion and epithelial inflammation, respectively. Graphical Abstract Figure. Lactobacilli need physical contact with pathogens and vaginal epithelia to reduce toxin secretion and epithelial inflammation, respectively.