Frank C. Gibson III, Ph.D.

Frank Gibson, Associate Professor, Department of Oral Biology

Associate Professor

Department of Oral Biology
1395 Center Drive, DG-56
Box 100424
Gainesville, FL, 32610-0424
Phone: 352-273-8856
Email: fgibson@dental.ufl.edu

 

 

 

  • Ph.D. University of New Hampshire, Durham, NH    Microbiology, 1994
  • B.S.   University of New Hampshire, Durham, NH    Biology, 1989

Research Interests

  • ŸHost-Pathogen Interaction
  • Inflammation
  • Infection and Systemic Disease
  • Bacterial Pathogenesis

Main Interests

Research in my lab is focused in areas of host-pathogen interaction geared toward developing a better understanding of the host mechanisms and bacterial structures important in infection-elicited inflammation.  To accomplish this we use a variety of approaches including molecular, cellular, immunological, and animal modeling to develop a synthetic understanding of relevant systems.  Work has centered on identification of host cell receptors engaged by key bacterial structures/adhesins, and the subsequent signaling pathways activated which lead to immune activation, with the goal to harness those factors in a manner that can lead to re-establishment of normal tissue homeostasis.  Current investigative lines utilize the bacterium Porphyromonas gingivalis as a model oral organism to study key facets of anaerobic bacterial infection and contribution of bacterial structures such as capsular polysaccharides in the development of inflammation and oral bone loss.  A particular area of interest is identification of molecular targets and pathways that could serve as novel points for therapeutic intervention to augment available treatments aimed to limit periodontal tissue destruction.

In addition to the work focusing on the pathogenesis of oral disease, our group engaged in collaborative studies that have been seminal in identifying associations of oral bacterial infection with cardiovascular disease.  Work in this area provides experimental evidence that P. gingivalis is a potential risk factor for atherosclerosis, and that this infection-elicited acceleration can be prevented through immunization.  The underlying mechanisms of this association are not well defined.  More recently we have become interested in nuclear hormone receptors including liver x receptors and peroxisome proliferator-activated receptors in the development of bacteria-elicited inflammation, and contribution of inflammatory cues at sites of infection in the pathogenesis of periodontal disease.  Furthermore, collaborative studies have begun to explore P. gingivalis interactions with adipocytes, as well as integrative studies to investigate aspects of P. gingivalis / HIV co-infection.

Select Publications

  • Papadopoulos G, Shaik-Dasthagirisaheb YB, Huang N, Viglianti GA, Henderson AJ, Kantarci A, Gibson FC 3rd. Immunologic environment influences macrophage response to Porphyromonas gingivalis. Mol. Oral Microbiol. 2016.
  • Shaik-Dasthagirisaheb YB, Mekasha S, He X, Gibson FC 3rd, Ingalls RR. Signaling events in pathogen-induced macrophage foam cell formation. Pathog. Dis. 2016. 74(6).
  • Huang N, Shaik-Dasthagirisaheb YB, LaValley MP, Gibson FC 3rd. Liver x receptors contribute to periodontal pathogen-elicited inflammation and oral bone loss. Mol. Oral Microbiol. 2015. 30(6):438-50.
  • Shaik-Dasthagirisaheb YB, Huang N, Weinberg EO, Shen SS, Genco CA, Gibson FC 3rd. Aging and contribution of MyD88 and TRIF to expression of TLR pathway-associated genes following stimulation with Porphyromonas gingivalis. J. Periodontal. Res. 2015. 50(1):89-102.
  • Shaik-Dasthagirisaheb YB, Huang N, Gibson FC 3rd. Inflammatory response to Porphyromonas gingivalis partially requires interferon regulatory factor (IRF) 3.Innate Immun. 2014. 20(3):312-9.
  • Papadopoulos G, Weinberg EO, Massari P, Gibson FC 3rd, Wetzler LM, Morgan EF, Genco CA. Macrophage-specific TLR2 signaling mediates pathogen-induced TNF-dependent inflammatory oral bone loss. J. Immunol. 2013. 190(3):1148-57.
  • Shaik-Dasthagirisaheb YB, Huang N, Baer MT, Gibson FC 3rd. Role of MyD88-dependent and MyD88-independent signaling in Porphyromonas gingivalis-elicited macrophage foam cell formation. Mol. Oral Microbiol. 2013. 28(1):28-39.
  • Hayashi C, Viereck J, Hua N, Phinikaridou A, Madrigal AG, Gibson FC 3rd, Hamilton JA, Genco CA. Porphyromonas gingivalis accelerates inflammatory atherosclerosis in the innominate artery of ApoE deficient mice. Atherosclerosis. 2011. 215(1):52-9.
  • Shaik-Dasthagirisaheb YB, Kantarci A, Gibson FC 3rd. Immune response of macrophages from young and aged mice to the oral pathogenic bacterium Porphyromonas gingivalis. Immun. Ageing. 2010. 7:15.
  • Baer MT, Huang N, Gibson FC 3rd. Scavenger receptor A is expressed by macrophages in response to Porphyromonas gingivalis, and participates in TNF-alpha expression. Oral Microbiol. Immunol. 2009. 24(6):456-63.
  • Liu X, Ukai T, Yumoto H, Davey M, Goswami S, Gibson FC 3rd, Genco CA. Toll-like receptor 2 plays a critical role in the progression of atherosclerosis that is independent of dietary lipids. Atherosclerosis. 2008. 196(1):146-54.
  • d’Empaire G, Baer MT, Gibson FC 3rd. The K1 serotype capsular polysaccharide of Porphyromonas gingivalis elicits chemokine production from murine macrophages that facilitates cell migration. Infect Immun. 2006. 74(11):6236-43.
  • Gibson FC 3rd, Hong C, Chou HH, Yumoto H, Chen J, Lien E, Wong J, Genco CA. Innate immune recognition of invasive bacteria accelerates atherosclerosis in apolipoprotein E-deficient mice. Circulation. 2004. 109(22):2801-6.
  • Gibson FC 3rd, Gonzalez DA, Wong J, Genco CA. Porphyromonas gingivalis-specific immunoglobulin G prevents P. gingivalis-elicited oral bone loss in a murine model. Infect Immun. 2004. 72(4):2408-11.
  • Gyurko R, Boustany G, Huang PL, Kantarci A, Van Dyke TE, Genco CA, Gibson FC 3rd. Mice lacking inducible nitric oxide synthase demonstrate impaired killing of Porphyromonas gingivalis. Infect Immun. 2003. 71(9):4917-24.
  • Gonzalez D, Tzianabos AO, Genco CA, Gibson FC 3rd. Immunization with Porphyromonas gingivalis capsular polysaccharide prevents P. gingivalis-elicited oral bone loss in a murine model. Infect Immun. 2003. 71(4):2283-7.
  • Chae P, Im M, Gibson F, Jiang Y, Graves DT. Mice lacking monocyte chemoattractant protein 1 have enhanced susceptibility to an interstitial polymicrobial infection due to impaired monocyte recruitment. Infect Immun. 2002. 70(6):3164-9.
  • Gibson FC 3rd, Genco CA. Prevention of Porphyromonas gingivalis-induced oral bone loss following immunization with gingipain R1. Infect Immun. 2001. 69(12):7959-63.
  • Gibson FC 3rd, Onderdonk AB, Kasper DL, Tzianabos AO. Cellular mechanism of intraabdominal abscess formation by Bacteroides fragilis. J. Immunol. 1998. 160(10):5000-6.
  • Cisneros RL, Gibson FC 3rd, Tzianabos AO. Passive transfer of poly-(1-6)-beta-glucotriosyl-(1-3)-beta-glucopyranose glucan protection against lethal infection in an animal model of intra-abdominal sepsis. Infect Immun. 1996. 64(6):2201-5.
  • Gibson FC 3rd, Tzianabos AO, Onderdonk AB. The capsular polysaccharide complex of Bacteroides fragilis induces cytokine production from human and murine phagocytic cells. Infect Immun. 1996. 64(3):1065-9.
  • Gibson FC 3rd, Tzianabos AO, Rodgers FG. Adherence of Legionella pneumophila to U-937 cells, guinea-pig alveolar macrophages, and MRC-5 cells by a novel, complement-independent binding mechanism. Can J Microbiol. 1994 40(10):865-72.