Seminal plasma promotes Neisseria gonorrhoeae aggregation and biofilm formation

Mark T. Anderson, Luke Byerly, Michael A. Apicella, H. Steven Seifert*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

18 Scopus citations

Abstract

Neisseria gonorrhoeae causes the human-specific disease gonorrhea and is transmitted from person to person primarily via sexual contact. During transmission, N. gonorrhoeae is often exposed to seminal fluid and must adapt to this change in environment. Previous work demonstrated that seminal fluid facilitates N. gonorrhoeae motility and alters epithelial cell interactions. In this study, exposure to seminal fluid was found to decrease surface adherence of gonococci in a manner that was independent of Opa adhesin proteins or type IV pilus retraction. Semen was also shown to cause dispersal of bacteria that had previously established surface adherence. Although surface adherence decreased, interbacterial interactions were increased by seminal plasma both in long-term static culture and on a cell-to-cell basis over shorter time periods. The result of increased bacterium-bacterium interactions resulted in the formation of microcolonies, an important step in the N. gonorrhoeae infectious process. Seminal fluid also facilitated increased bacterial aggregation in the form of shear-resistant three-dimensional biofilms. These results emphasize the importance of the gonococcal response to the influx of seminal fluid within the genital niche. Further characterization of the N. gonorrhoeae response to semen will advance our understanding of the mechanisms behind the establishment of infection in naive hosts and the process of transmission.

Original languageEnglish (US)
Pages (from-to)2228-2235
Number of pages8
JournalJournal of bacteriology
Volume198
Issue number16
DOIs
StatePublished - 2016

Funding

This work, including the efforts of H. Steven Seifert and Mark T. Anderson, was funded by HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID) (R01 AI044239). This work, including the efforts of H. Steven Seifert and Mark T. Anderson, was funded by HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID) (R37 AI033493). This work, including the efforts of Michael A. Apicella, was funded by HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID) (R21 AI109320).

ASJC Scopus subject areas

  • Molecular Biology
  • Microbiology

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