Janina Lewis
Virginia Commonwealth University, VA·Microbiology & Immunology
The mouth is full of nitrite and nitric oxide, chemicals that act as signaling molecules and can damage bacteria. They create what is called nitrosative stress.
- Fields
Microbiology & Immunology
Biochemistry
Medicine & Clinical Research
- Topics
Porphyromonas gingivalis
periodontal disease
periodontitis
- Grants
- 1 known grant, through Aug 2027
What they work on
- Define how Porphyromonas gingivalis senses nitrosative stress by determining the structure and biochemistry of HcpR, a regulator that uses a hemin-dependent mechanism to switch on the hcp gene.
- Use proteomics to catalog the S-nitrosylome, the set of proteins tagged with nitric oxide groups by the S-nitrosylase enzyme Hcp, in P. gingivalis under nitrosative stress.
- Determine the mechanism by which Hcp protects P. gingivalis from nitrite and nitric oxide, and identify other regulatory and effector proteins that help defend the bacterium against nitrosative stress.
- Verify that the HcpR-Hcp system and related defense mechanisms contribute to P. gingivalis survival in host-pathogen settings that model infection.
More about the research
Nitrite in the mouth can reach very high levels, and inflamed gum tissue releases more nitric oxide. Bacteria that cause gum (periodontal) disease must therefore cope with this stress to survive. Porphyromonas gingivalis, a major bacterium behind periodontal disease, tolerates nitrosative stress very well, but how it does so is largely unknown. This project asks how P. gingivalis senses and defends against nitrosative stress. The longer-term aim is to block those defenses so the body's own nitrite and nitric oxide stop the bacterium from growing.
Why it matters
Adult periodontal disease is driven in part by Porphyromonas gingivalis. Knowing how this bacterium survives nitrite and nitric oxide could point to agents that disable its defenses and let the body's own nitrosative chemicals block its growth. This could open new ways to treat and prevent gum disease. The findings may also apply to other bacteria that use similar protection systems.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Hansel Fletcher
Loma Linda University, CA·Microbiology & Immunology
Determine the sequential post-translational processing steps that convert inactive progingipains into mature gingipain complexes on the Porphyromonas gingivalis surface.
Ping Zhang
University of Alabama at Birmingham, AL·Microbiology & Immunology
Determine how periodontitis regulates activation of microglia, the brain's resident immune cells, in Alzheimer's disease model mice, using three different experimental models of periodontal disease.
Fata Moradali
University of Louisville, KY·Microbiology & Immunology
Compare the chemical structure of lipopolysaccharide from wild-type P. gingivalis strain 381 with that from mutants lacking the c-di-AMP-degrading enzyme pdepg or the regulator cdaR, using large-scale purification, chromatographic fractionation, FLATn, MALDI-ToF mass spectrometry, and NMR.
The school
Virginia Commonwealth University: 19 labs on PI Pages, $524M a year on research, 438 research doctorates a year.
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