Joseph Dillard
University of Wisconsin-Madison, WI·Microbiology & Immunology
Gonorrhea is caused by the bacterium Neisseria gonorrhoeae, and much of the harm it does to patients comes not from the bacterium directly but from the immune reaction it provokes. In the upper female reproductive tract this inflammation kills the hair-like ciliated cells that move an egg down the Fallopian tube, raising the risk of ectopic pregnancy and infertility, and leaves scar-like adhesions that tear and cause chronic pelvic pain.
- Fields
Microbiology & Immunology
Genetics
Medicine & Clinical Research
- Topics
Neisseria gonorrhoeae
gonorrhea
peptidoglycan
- Grants
- 2 known grants, through May 2028
What they work on
- Define the biochemical function of NlpC, a gonococcal D,L-endopeptidase that cuts the cell wall mesh, and determine how it changes the peptidoglycan fragments released and the structure of the wall itself.
- Determine where in the Neisseria gonorrhoeae cell NlpC acts and which other peptidoglycan-related proteins it interacts with, using mutants deficient in NlpC expression.
- Measure how the muramyl dipeptide-like fragment that activates the human sensor NOD2 alters cytokine and chemokine responses, using organ cultures of human Fallopian tube and cervix and cultured male urethral cells.
- Test whether the Gardnerella toxin vaginolysin, which lyses epithelial cells in a CD59-dependent manner, promotes sialylation of gonococcal lipooligosaccharide and thereby factor H recruitment and complement resistance.
- Test whether sialidase from some Gardnerella species strips sialic acid from gonococcal lipooligosaccharide to enable binding to asialoglycoprotein receptors on endometrial and male urethral cells, using targeted Gardnerella mutants and complemented strains.
More about the research
Both grants ask how this damage gets started: one dissects the bacterial cell-wall fragments that trigger the inflammation, the other asks how bacteria already living in the vagina help gonococci survive and spread.
Why it matters
Gonorrhea's worst outcomes in women, pelvic inflammatory disease, ectopic pregnancy, tubal-factor infertility and chronic pelvic pain, trace back to inflammation and to the bacterium's ability to evade immune killing and transmit. Identifying the enzymes and cell wall fragments that drive the damaging NOD2 response, and the Gardnerella factors that help gonococci survive, could point to targets for blocking tissue injury and for reducing how bacterial vaginosis amplifies the spread of gonorrhea and other sexually transmitted infections.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Kathryn Frietze
University of New Mexico, NM·Microbiology & Immunology
Engineer bacteriophage virus-like particle vaccines, virus shells that display a chosen protein fragment in a repeating array, to raise high levels of antibodies against Chlamydia trachomatis adhesion factors, and measure their immunogenicity in mouse immunization studies.
Jeonghoon Lee
University of Nebraska Medical Center, NE·Microbiology & Immunology
Test whether Pkn1, a serine/threonine kinase of Chlamydia trachomatis, controls recruitment of cell-division components to the septum, using an anhydrotetracycline-inducible, histidine-tagged Pkn1 and CRISPR interference knockdown of pkn1.
Diane Edmondson
University of Texas Health Science Center at Houston, TX·Microbiology & Immunology
Define the nutritional requirements of Treponema pallidum, the spiral bacterium that causes syphilis, using metabolomic profiling and systematic nutrient testing to build an experimentally validated metabolic map.
The school
University of Wisconsin-Madison: 91 labs on PI Pages, $1.9B a year on research, 854 research doctorates a year.
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