Phone¬† (317) 278-1936
Fax¬†¬†¬†¬†¬†¬† (317) 278-1411
Indiana University School of Dentistry
Department of¬†Biomedical and Applied Sciences
1121 West Michigan Street, Room 261
Indianapolis, Indiana¬† 46202
M.S. in Biology, Ludwig Maximiliams-Universit√§t, Munich, Germany
PhD. in Microbiology, Ludwig Maximiliams-Universit√§t, Munich, Germany
Postdoctoral Fellowship, University of Texas Health Science Center, San Antonio, TX
Wahaidi, Y.Y., G.J. Eckert, R.L. Gregory, M.J. Kowolik, and D.M. Galli. The in-vitro response of human peripheral blood neutrophils to Fusobacterium nucleatum. Int J Clin Dent 6(1), accepted.
Wahaidi, V.Y., M. J. Kowolik, G.J. Eckert and D. M. Galli. 2011. Endotoxemia and the host systemic response during experimental gingivitis.¬† J Clin Periodontol 38:412-417.
Srinivasan, M., Kodumudi, K.N., and D.M. Galli. 2010. Aggregatibacter actinomycetemcomitans modulates toll like receptors 2 and 4 in gingival epithelial cells in experimental periodontitis. J Int Clin Dent Res Org 2(1): 24-29.¬†
Chen, J., Pappas, D.L., and D. M. Galli. 2010. Mapping of the nick site on conjugative plasmid pVT745 by interrupted mating. Plasmid 63: 136-142.
Wilder, R.S., O‚ÄôDonnell, J.A., Barry, M., Galli, D.M., Hakim, F.F., Holyfield, L.J., and M.R. Robbins. 2008. Is dentistry at risk? A case for interprofessional education. J Dent Edu 72(11): 1231-1237.
Galli, D.M., and J. Chen. 2006. Entry exclusion activity on conjugative plasmid pVT745. Plasmid, 55(2):158-163.
Permpanich, P., Kowolik, M., and D.M. Galli.¬† 2006. Resistance of fluorescent-labeled Actinobacillus actinomycetemcomitans strains to phagocytosis and killing by human neutrophils Cell. Microbiol, 8(1):72-84.
Chen, J., LeBlanc, D. J., and D. M. Galli. 2002. DNA inversion on conjugative plasmid pVT745. J. Bacteriol. 184:5926-5934.
Galli, D. M., Kerr, M. S., Fair, A. D., Permpanich, P., and D. J. LeBlanc. 2002. Parameters associated with cloning in Actinobacillus actinomycetemcomitans. Plasmid 47: 138-147.
Galli, D.M., Chen, J., Novak, K.F., and LeBlanc, D.J. 2001. Nucleotide sequence and analysis of conjugative plasmid pVT745. J. Bacteriol. 183:1585-1594.
Galli, D.M., and LeBlanc, D.J. 1997. Identification of a maintenance system on rolling circle replicating plasmid pVT736-1. Mol. Microbiol. 25:649-659.
Galli, D.M., Polan-Curtain, J.L., and LeBlanc, D.J. 1996. Structural and segregational stability of various replicons in Actinobacillus actinomycetemcomitans. Plasmid 36:42-48.
Galli, D.M., and LeBlanc, D.J. 1995. Transcriptional analysis of rolling circle replicating plasmid pVT736-1: Evidence for replication control by antisense RNA. J. Bacteriol. 177:4474-4480.
Galli, D.M. and LeBlanc, D.J. 1994. Characterization of pVT736-1, a rolling circle DNA plasmid from the gram-negative bacterium Actinobacillus actinomycetemcomitans. Plasmid 31:148-157.
Muscholl, A., D. Galli, G. Wanner, and R. Wirth. 1993. Sex pheromone plasmid pAD1-encoded aggregation substance of Enterococcus faecalis is positively regulated in trans by the traE1 gene product. Eur J Biochem 214: 333-338.
Hirt, H., G. Wanner, D. Galli, and R. Wirth. 1993. Biochemical, immunological, and ultrastructural characterization of aggregation substances encoded by Enterococcus faecalis¬† sex pheromone plasmids. Eur J Biochem 211: 711-716.
Galli, D., A. Friesenegger, and R. Wirth. 1992. Transcriptional control of sex pheromone-inducible genes on plasmid pAD1 of Enterococcus faecalis¬† and sequence analysis of a third structural gene for (pPD1-encoded) aggregation substance. Mol Microbiol 6: 1297-1308.
Weidlich, G., R. Wirth, and D. Galli. 1992. Sex pheromone plasmid pAD1-encoded surface exclusion protein of Enterococcus faecalis. Mol Gen Genet 233: 161-168.
Wirth, R., S. Olmsted, D. Galli, and G. Dunny. 1991. Comparative analysis of cAD1- and cCF10-induced aggregation substances of Enterococcus faecalis, p. 34-38. In G. M. Dunny, P. P. Cleary, and L. L. McKay (ed.), Genetics and molecular biology of streptococci, lactococci, and enterococci. American Society for Microbiology, Washington, D.C.
Galli, D., and R. Wirth. 1991. Comparative analysis of Enterococcus faecalis sex pheromone plasmids identifies a single homologous DNA region which codes for aggregation substance. J Bacteriol 173: 3029-3033.
Wirth, R., G. Wanner, and D. Galli. 1990. Das Sex Pheromon System von Enterococcus faecalis: ein einzigartiger Mechanismus zum Aufsammeln von Plasmiden. Forum Mikrobiol 6: 321-332.
Galli, D., F. Lottspeich, and R. Wirth. 1990. Sequence analysis of Enterococcus faecalis aggregation substance encoded by the sex pheromone plasmid pAD1. Mol Microbiol 4: 895-904.
Wanner, G., Formanek, H., Galli, D., and R. Wirth. 1989. Localization of aggregation substances of Enterococcus faecalis after induction by sex pheromones. Arch Microbiol 151: 491-497.
Galli, D., R. Wirth, and G. Wanner. 1989. Identification of aggregation substances of Enterococcus faecalis after induction by sex pheromones. Arch Microbiol 151: 486-490.
In collaboration with Dr. Michael Kowolik, our goal is to understand the mechanisms whereby oral infection and local inflammation may impact cardiovascular and other inflammatory disease risk. While the mainstream focus for the past 20 years has been on the systemic impact of periodontitis, ours has been to harness a controlled model of human oral infection, the ‚ÄúExperimental Gingivitis Model‚ÄĚ. This model permits investigator control of induced infection and resolution of gingivitis, and to determine a range of systemic (or local) microbial and host outcomes. We are the first to demonstrate a systemic inflammatory response under the conditions of the 21-day model and, significantly, that the accumulation of dental plaque in systemically healthy young adults results in endotoxemia, a known driver of atherogenesis. Our specific areas of interest are i) to better understand the extent of gingivitis-induced endotoxemia/bacteremia, ii) to characterize the systemic inflammatory response to bacteria and/or their cell products, iii) to assess susceptibility to systemic infection and inflammation at the genetic level, and iv) to determine how the systemic response to oral infection impacts the vascular endothelium.
Microbial contamination of dental unit waterlines
Dental unit waterlines favor the formation of microbial biofilms due to low flow rates, stagnation and low shear stresses from the small diameter tubing of the lines. Bacterial species associated with these biofilms are derived from municipal waters. The biofilms resist treatment with disinfectants and can harbor waterborne pathogens such as Legionella pneumophila and, as we showed recently, Helicobacter pylori, thus posing an infection risk to both patients and dental staff. Detection of biofilm bacteria requires microscopic or molecular biology techniques since only 3-5% of microorganisms in the water are cultivable. Current standards to assess water quality are based on bacterial culture only. Our goal is twofold: i) the development of a new method for water quality testing that is independent of culture, reliable and quick; and ii) the prevention of biofilm formation in dental unit waterlines (treatment of water and/or waterline material). We are in the process of developing an in vitro model with a mobile dental unit that allows us to mimic the clinical chair set up in the laboratory.
The role of Aggregatibacter actinomycetemcomitans in periodontal and systemic disease
Aggregatibacter (formerly Actinobcacillus) actinomycetemcomitans (Aa) is a Gram-negative facultative, capnophylic, coccobacillus found in the oral cavities of healthy and periodontally affected individuals. The organism has been implicated as the causative agent of aggressive periodontitis as well as other types of human infections. Aa is also a member of a clinically important group of bacteria, the HACEK group that is responsible for 3-10% of cases of infective endocarditis. For a long time a thorough study of Aa virulence traits was hampered due to the lack of an appropriate genetic system. In recent years, the core of our research has focused on the use of plasmids and other mobile genetic elements to develop molecular biological and genetic tools that will allow for an investigation of the functionality and regulation of putative Aa virulence traits.