J Fenno
University of Michigan, MI·Microbiology & Immunology
Gum disease, or periodontitis, destroys the tissue and bone that hold teeth in place, and it begins when the mix of bacteria in the mouth shifts out of balance. One of the bacteria enriched in diseased sites is Treponema denticola, a corkscrew-shaped oral spirochete related to the organism that causes syphilis.
- Fields
Microbiology & Immunology
Biology
Medicine & Clinical Research
- Topics
Treponema denticola
spirochete
periodontal disease
- Grants
- 1 known grant, through Jan 2027
What they work on
- Characterize how dentilisin, a protease complex built on the PrtP lipoprotein, and the oligomeric Msp protein are assembled in the Treponema denticola outer membrane, using purified native and recombinant proteins.
- Determine how specific domains of dentilisin and Msp, plus bacterial lipooligosaccharide, disrupt TLR/MyD88 microbe-sensing and integrin/FAK adhesion signaling in cultured periodontal ligament cells, using isogenic mutant strains.
- Measure the downstream consequences of T. denticola challenge for the host cytoskeleton and for expression and activity of matrix metalloproteinases, the enzymes that degrade connective tissue.
- Test how much individual T. denticola surface components contribute to tissue destruction in a mouse model of periodontal disease.
- Test whether the antimicrobial peptide nisin can modulate T. denticola-induced dysbiotic signaling in both periodontal cell cultures and the mouse periodontal disease model.
More about the research
The question driving this work is how proteins on the surface of this bacterium touch and reprogram human tissue, and how that contact starts and sustains disease. The focus is the periodontal ligament, the tissue layer that joins the tooth root to the bone of the tooth socket.
Why it matters
Periodontitis is a common chronic infection that destroys the attachment between teeth and bone. Pinpointing the bacterial surface proteins that disrupt tissue-maintenance pathways in the periodontal ligament could identify targets for blocking tissue breakdown, and tests of the antimicrobial peptide nisin may indicate whether such a compound could calm disease-driving signaling. The work also adds basic knowledge about spirochetes and about how microbes drive chronic infections generally.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Yingzi Yang
Harvard University, MA·Genetics
Characterize periodontal crestal stem cells, including Gli1+ cells that report Hedgehog signaling activity, and determine how they are activated by injury in the upper rim of the tooth socket where bone, ligament and gum meet.
Janina Lewis
Virginia Commonwealth University, VA·Microbiology & Immunology
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.
Adam Lietzan
University of North Carolina at Chapel Hill, NC·Microbiology & Immunology·Early-career
Identify the cellular pathways that interleukin-37 (IL-37), an anti-inflammatory cytokine, changes in oral epithelial cells challenged with microbes, using in vitro and in vivo models.
The school
University of Michigan: 124 labs on PI Pages, $2.1B a year on research, 963 research doctorates a year.
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