Fata Moradali
University of Louisville, KY·Microbiology & Immunology
Periodontitis is a common inflammatory disease that destroys the gum and bone tissue holding teeth in place, and it is driven by communities of bacteria living in pockets around the tooth. One species, Porphyromonas gingivalis, is strongly linked to the start and progression of the disease.
- Fields
Microbiology & Immunology
Biochemistry
Medicine & Clinical Research
- Topics
periodontitis
Porphyromonas gingivalis
lipopolysaccharide
- Grants
- 1 known grant, through Aug 2029
What they work on
- 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.
- Map the protein interaction network behind c-di-AMP control of lipopolysaccharide and identify the receptors and effectors that bind this bacterial second messenger, using genetic and biochemical approaches.
- Confirm the importance of newly identified interaction partners by mutating their genes in P. gingivalis and measuring the resulting changes in lipopolysaccharide structure and function.
- Test whether purified lipid A and lipopolysaccharide fractions from wild-type and mutant bacteria differ in how strongly they trigger TLR4 signaling, complement activation, and cytokine production, using cell culture, human whole blood, and an animal inflammation model.
More about the research
Its outer surface carries lipopolysaccharide, a large molecule of sugars and fats that the human immune system detects and reacts to, sometimes with damaging inflammation. Work from this laboratory first showed that P. gingivalis adjusts the structure, and therefore the activity, of this surface molecule using c-di-AMP, a small internal messenger that bacteria use to coordinate their own behavior. Because mammals do not make or use c-di-AMP, the pathway is attractive as a drug target that would leave host cells untouched.
Why it matters
Periodontitis affects roughly half of U.S. adults and carries large social and economic costs, yet treatment still relies mostly on mechanical cleaning and antibiotics. By explaining how a bacterial signaling system absent from human cells tunes the inflammatory strength of P. gingivalis, this work could identify a druggable target for blocking the bacterium's adaptation to the gum pocket without disturbing the patient's own biology.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
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.
Jose Lemos
University of Florida, FL·Microbiology & Immunology
Uncover the regulatory mechanisms that let Streptococcus mutans tolerate high zinc, focusing on ZccE, a zinc-exporting pump unique to this species, and its regulator ZccR, using genetic and mutational approaches.
The school
University of Louisville: 15 labs on PI Pages, $225M a year on research, 159 research doctorates a year.
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