P06.09 Lactobacillus crispatus inhibits growth of gardnerella vaginalis and neisseria gonorrhoeae on a porcine vaginal mucosa model

Introduction The vaginal microbiota affects susceptibility to bacterial vaginosis (BV) and sexually transmitted infections (STIs). BV is characterised by depletion of Lactobacillus spp., an overgrowth of anaerobes (usually dominated by Gardnerella vaginalis ) and a pH > 4.5. BV is associated with an increased risk of acquiring STIs such as chlamydia and gonorrhoea. An ex vivo porcine vaginal mucosal model (PVM) was developed to explore the mechanistic role of Lactobacillus in affecting vaginal colonisation by G. vaginalis and Neisseria gonorrhoeae . Methods Explants (5 mm) of freshly collected PVM were placed in transwells over various media, including Lactobacillus culture supernatant, inoculated with bacteria and incubated under aerobic or anaerobic conditions. Colonised explants were processed for CFU enumeration and presence of biofilm (via confocal microscopy) at indicated times. Lactic acid produced by a clinical isolate of L. crispatus growing on PVM was also quantified. Results All isolates tested could colonise and grow on PVM. G. vaginalis and N. gonorrhoeae form biofilms on PVM. L. crispatus produces lactic acid on PVM and inhibits the growth of N. gonorrhoeae and G. vaginalis in a pH-dependent manner. Finally, L. crispatus produces a secreted factor that kills N. gonorrhoeae on PVM at an otherwise permissible pH. Conclusion These data demonstrate that PVM is a useful model for studying the interactions of commensal vaginal microbes with pathogens on the vaginal mucosa. The data confirm a role for lactic acid in inhibiting growth of G. vaginalis and N. gonorrhoeae . The discovery of an L. crispatus secreted factor that kills N. gonorrhoeae is intriguing and future work will identify this compound and explore its mechanism of action. Disclosure of interest statement Funding provided by the Office of the Vice President for Research, University of Minnesota and NIH grant U19AI084044. No pharmaceutical grants were received in the development of this study.