Induction of Innate Immune Responses by Commensal and Pathogenic Neisseria Species

Abstract

Neisseria gonorrhoeae, the etiological agent of gonorrhea, infects over 62 million people annually worldwide. Many of these infections occur asymptomatically, demonstrating that N. gonorrhoeae can infect mucosal epithelia without causing overt disease. The Neisseria genus also contains over eight commensal species, which by definition, are capable of colonizing host cells without causing disease. These findings indicate that Neisseria species have developed strategies for minimizing the host immune response to infection. To investigate these strategies we infected endocervical and nasopharyngeal epithelial cells with N. gonorrhoeae, a pathogen, or N. elongata, a commensal. We then compared protein levels of two different transcriptional regulators, NFκB and ATF3. These represent two different signaling pathways involved in regulating the innate immune response. We found that both species were able to increase levels of both NFκB and ATF3. In addition, we tested the role of type IV pilus (Tfp) retraction in the upregulation of ATF3 during infection with both species. We found little evidence that Tfp retraction plays a role in ATF3 upregulation. Responses to infection with the pathogen and commensal varied by cell type. We conclude that both the pathogen and commensal alter host cell signaling pathways in order to establish asymptomatic infections.