Lactobacillus crispatus inhibits growth of Gardnerella vaginalis and Neisseria gonorrhoeae on a porcine vaginal mucosa model

Laura M. Breshears, Vonetta L. Edwards, Jacques Ravel, Marnie L. Peterson

Research output: Contribution to journalArticlepeer-review

88 Scopus citations


Background: The vaginal microbiota can impact the susceptibility of women to bacterial vaginosis (BV) and sexually transmitted infections (STIs). BV is characterized by depletion of Lactobacillus spp., an overgrowth of anaerobes (often dominated by Gardnerella vaginalis) and a pH > 4.5. BV is associated with an increased risk of acquiring STIs such as chlamydia and gonorrhea. While these associations have been identified, the molecular mechanism(s) driving the risk of infections are unknown. An ex vivo porcine vaginal mucosal model (PVM) was developed to explore the mechanistic role of Lactobacillus spp. in affecting colonization by G. vaginalis and Neisseria gonorrhoeae. Results: The data presented here demonstrate that all organisms tested can colonize and grow on PVM to clinically relevant densities. Additionally, G. vaginalis and N. gonorrhoeae form biofilms on PVM. It was observed that lactic acid, acetic acid, and hydrochloric acid inhibit the growth of G. vaginalis on PVM in a pH-dependent manner. N. gonorrhoeae grows best in the presence of lactic acid at pH 5.5, but did not grow well at this pH in the presence of acetic acid. Finally, a clinical Lactobacillus crispatus isolate (24-9-7) produces lactic acid and inhibits growth of both G. vaginalis and N. gonorrhoeae on PVM. Conclusions: These data reveal differences in the effects of pH, various acids and L. crispatus on the growth of G. vaginalis and N. gonorrhoeae on a live vaginal mucosal surface. The PVM is a useful model for studying the interactions of commensal vaginal microbes with pathogens and the mechanisms of biofilm formation on the vaginal mucosa.

Original languageEnglish (US)
Article number276
JournalBMC microbiology
Issue number1
StatePublished - Dec 9 2015

Bibliographical note

Funding Information:
We would like to thank Dr. Michele Anderson for helpful discussions, Heidi Wang for technical assistance and Mark Sanders for imaging support. This work was funded with support from the Office of the Vice President for Research, University of Minnesota. The research reported in this publication was supported in part by the National Institute of Allergy and Infectious Diseases of the National Institutes of Health under award number U19AI084044. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Publisher Copyright:
© 2015 Breshears et al.


  • Bacterial vaginosis
  • Biofilm
  • Lactobacillus
  • Microbiota
  • Sexually transmitted infections
  • Vaginal explants
  • Vaginal mucosa


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