Induction of Innate Immune Responses by Commensal and Pathogenic Neisseria Species

Persistent Link:
http://hdl.handle.net/10150/244816
Title:
Induction of Innate Immune Responses by Commensal and Pathogenic Neisseria Species
Author:
Wade, Laura Katherine
Issue Date:
May-2012
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
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.
Type:
text; Electronic Thesis
Degree Name:
B.S.H.S.
Degree Level:
bachelors
Degree Program:
Honors College; Physiology
Degree Grantor:
University of Arizona

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titleInduction of Innate Immune Responses by Commensal and Pathogenic Neisseria Speciesen_US
dc.creatorWade, Laura Katherineen_US
dc.contributor.authorWade, Laura Katherineen_US
dc.date.issued2012-05-
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractNeisseria 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.en_US
dc.typetexten_US
dc.typeElectronic Thesisen_US
thesis.degree.nameB.S.H.S.en_US
thesis.degree.levelbachelorsen_US
thesis.degree.disciplineHonors Collegeen_US
thesis.degree.disciplinePhysiologyen_US
thesis.degree.grantorUniversity of Arizonaen_US
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