Abstract

Neisseria gonorrhoeae (Gc) is a sexually transmitted infectious agent that is the only causative agent of the disease gonorrhea. As a strict human pathogen, this bacterium has evolved sophisticated mechanisms to facilitate colonization and growth within affected human populations and its spread. Central to the disease gonorrhea is the massive influx of white cells that occurs in both males and females during symptomatic Gc infection. This """"""""purulent exudate"""""""" consists predominately of human polymorphonuclear lymphocytes (PMNs) with associated viable Gc. The interplay between Gc and the PMN is an essential part of pathogenesis. This competitive renewal will continue to explore the molecular mechanisms used by novel factors we have identified that are important for the interaction of Gc and PMNs, to uncover new mechanisms important for Gc survival within and among PMNs, and to determine how Gc modulates the apoptotic pathways of PMNs.

Public Health Relevance

Neisseria gonorrhoeae causes the disease gonorrhea and survives and modulates the anti- microbial actions of human polymorphonuclear lymphocytes (PMNs). This work will uncover new virulence factors important for N. gonorrhoeae survival within and among PMNs,and to determine how N. gonorrhoeae modulates PMN function.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Project (R01)
Project #
5R01AI044239-14
Application #
8434171
Study Section
Bacterial Pathogenesis Study Section (BACP)
Program Officer
Hiltke, Thomas J
Project Start
1998-12-01
Project End
2015-03-31
Budget Start
2013-04-01
Budget End
2014-03-31
Support Year
14
Fiscal Year
2013
Total Cost
$354,791
Indirect Cost
$122,141

  Institution

Name
Northwestern University at Chicago
Department
Microbiology/Immun/Virology
Type
Schools of Medicine
DUNS #
005436803
City
Chicago
State
IL
Country
United States
Zip Code
60611

  Publications

Lenz, Jonathan D; Stohl, Elizabeth A; Robertson, Rosanna M et al. (2016) Amidase Activity of AmiC Controls Cell Separation and Stem Peptide Release and Is Enhanced by NlpD in Neisseria gonorrhoeae. J Biol Chem 291:10916-33
Peak, Ian R; Chen, Adrienne; Jen, Freda E-C et al. (2016) Neisseria meningitidis Lacking the Major Porins PorA and PorB Is Viable and Modulates Apoptosis and the Oxidative Burst of Neutrophils. J Proteome Res 15:2356-65
Palmer, Guy H; Bankhead, Troy; Seifert, H Steven (2016) Antigenic Variation in Bacterial Pathogens. Microbiol Spectr 4:
Château, Alice; Seifert, H Steven (2016) Neisseria gonorrhoeae survives within and modulates apoptosis and inflammatory cytokine production of human macrophages. Cell Microbiol 18:546-60
Obergfell, Kyle P; Seifert, H Steven (2016) The Pilin N-terminal Domain Maintains Neisseria gonorrhoeae Transformation Competence during Pilus Phase Variation. PLoS Genet 12:e1006069
Gunderson, Carl W; Seifert, H Steven (2015) Neisseria gonorrhoeae elicits extracellular traps in primary neutrophil culture while suppressing the oxidative burst. MBio 6:
Stohl, Elizabeth A; Lenz, Jonathan D; Dillard, Joseph P et al. (2015) The Gonococcal NlpD Protein Facilitates Cell Separation by Activating Peptidoglycan Cleavage by AmiC. J Bacteriol 198:615-22
Rotman, Ella; Seifert, H Steven (2015) Neisseria gonorrhoeae MutS affects pilin antigenic variation through mismatch correction and not by pilE guanine quartet binding. J Bacteriol 197:1828-38
Gault, Joseph; Ferber, Mathias; Machata, Silke et al. (2015) Neisseria meningitidis Type IV Pili Composed of Sequence Invariable Pilins Are Masked by Multisite Glycosylation. PLoS Pathog 11:e1005162
Obergfell, Kyle P; Seifert, H Steven (2015) Mobile DNA in the pathogenic Neisseria. Microbiol Spectr 3:

Showing the most recent 10 out of 62 publications