Frank Gibson

Frank Gibson, Ph.D.

ASO PROF

Department: DN-ORAL BIOLOGY
Business Phone: (352) 273-8856
Business Email: fgibson@dental.ufl.edu

Research Profile

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.

Areas of Interest
  • Bacterial pathogenesis
  • Host-pathogen interaction
  • Infection and systemic disease
  • Inflammation

Publications

2020
Porphyromonas gingivalis Sphingolipid Synthesis Limits the Host Inflammatory Response.
Journal of dental research. 99(5):568-576 [DOI] 10.1177/0022034520908784. [PMID] 32105543.
2020
Virulence of the Pathogen Porphyromonas gingivalis Is Controlled by the CRISPR-Cas Protein Cas3.
mSystems. 5(5) [DOI] 10.1128/mSystems.00852-20. [PMID] 32994292.
2020
Sphingolipid Containing Outer Membrane Vesicles Serve as a Delivery Vehicle to Limit Macrophage Immune Response to Porphyromonas gingivalis.
Infection and immunity. [DOI] 10.1128/IAI.00614-20. [PMID] 33361202.
2019
Immunization with cell-free-generated vaccine protects from Porphyromonas gingivalis-induced alveolar bone loss.
Journal of clinical periodontology. 46(2):197-205 [DOI] 10.1111/jcpe.13047. [PMID] 30578564.
2018
Linkage of Infection to Adverse Systemic Complications: Periodontal Disease, Toll-Like Receptors, and Other Pattern Recognition Systems.
Vaccines. 6(2) [DOI] 10.3390/vaccines6020021. [PMID] 29621153.
2016
Porphyromonas gingivalis-mediated signaling through TLR4 mediates persistent HIV infection of primary macrophages.
Virology. 499:72-81 [DOI] 10.1016/j.virol.2016.09.007. [PMID] 27639573.
2016
Signaling events in pathogen-induced macrophage foam cell formation.
Pathogens and disease. 74(6) [DOI] 10.1093/femspd/ftw074. [PMID] 27481727.
2015
Aging and contribution of MyD88 and TRIF to expression of TLR pathway-associated genes following stimulation with Porphyromonas gingivalis.
Journal of periodontal research. 50(1):89-102 [DOI] 10.1111/jre.12185. [PMID] 24862405.
2015
Liver X receptors contribute to periodontal pathogen-elicited inflammation and oral bone loss.
Molecular oral microbiology. 30(6):438-50 [DOI] 10.1111/omi.12103. [PMID] 25946408.
2014
Inflammatory response to Porphyromonas gingivalis partially requires interferon regulatory factor (IRF) 3.
Innate immunity. 20(3):312-9 [DOI] 10.1177/1753425913492180. [PMID] 23803413.
2014
Immuno-pathogenesis of Periodontal Disease: Current and Emerging Paradigms.
Current oral health reports. 1(2):124-132 [PMID] 24839590.
View on: PubMed
2013
Macrophage-specific TLR2 signaling mediates pathogen-induced TNF-dependent inflammatory oral bone loss.
Journal of immunology (Baltimore, Md. : 1950). 190(3):1148-57 [DOI] 10.4049/jimmunol.1202511. [PMID] 23264656.
2013
Role of MyD88-dependent and MyD88-independent signaling in Porphyromonas gingivalis-elicited macrophage foam cell formation.
Molecular oral microbiology. 28(1):28-39 [DOI] 10.1111/omi.12003. [PMID] 23194377.
2012
Protective role for TLR4 signaling in atherosclerosis progression as revealed by infection with a common oral pathogen.
Journal of immunology (Baltimore, Md. : 1950). 189(7):3681-8 [PMID] 22956579.
View on: PubMed
2011
Porphyromonas gingivalis accelerates inflammatory atherosclerosis in the innominate artery of ApoE deficient mice.
Atherosclerosis. 215(1):52-9 [DOI] 10.1016/j.atherosclerosis.2010.12.009. [PMID] 21251656.
2010
Immune response of macrophages from young and aged mice to the oral pathogenic bacterium Porphyromonas gingivalis.
Immunity & ageing : I & A. 7 [DOI] 10.1186/1742-4933-7-15. [PMID] 21114831.
2010
Pathogen-mediated inflammatory atherosclerosis is mediated in part via Toll-like receptor 2-induced inflammatory responses.
Journal of innate immunity. 2(4):334-43 [DOI] 10.1159/000314686. [PMID] 20505314.
2010
Review: Pathogen-induced inflammation at sites distant from oral infection: bacterial persistence and induction of cell-specific innate immune inflammatory pathways.
Molecular oral microbiology. 25(5):305-16 [DOI] 10.1111/j.2041-1014.2010.00582.x. [PMID] 20883220.
2009
Scavenger receptor A is expressed by macrophages in response to Porphyromonas gingivalis, and participates in TNF-alpha expression.
Oral microbiology and immunology. 24(6):456-63 [DOI] 10.1111/j.1399-302X.2009.00538.x. [PMID] 19832797.
2008
Bacterial fimbriae stimulate proinflammatory activation in the endothelium through distinct TLRs.
Journal of immunology (Baltimore, Md. : 1950). 180(4):2187-95 [PMID] 18250425.
View on: PubMed
2008
Engagement of specific innate immune signaling pathways during Porphyromonas gingivalis induced chronic inflammation and atherosclerosis.
Frontiers in bioscience : a journal and virtual library. 13:2041-59 [PMID] 17981690.
View on: PubMed
2008
Toll-like receptor 2 plays a critical role in the progression of atherosclerosis that is independent of dietary lipids.
Atherosclerosis. 196(1):146-154 [DOI] 10.1016/j.atherosclerosis.2007.03.025. [PMID] 17466307.
2008
Macrophage-elicited osteoclastogenesis in response to bacterial stimulation requires Toll-like receptor 2-dependent tumor necrosis factor-alpha production.
Infection and immunity. 76(2):812-9 [PMID] 17998311.
View on: PubMed
2007
Porphyromonas gingivalis mediated periodontal disease and atherosclerosis: disparate diseases with commonalities in pathogenesis through TLRs.
Current pharmaceutical design. 13(36):3665-75 [PMID] 18220804.
View on: PubMed
2006
Fimbria-dependent activation of pro-inflammatory molecules in Porphyromonas gingivalis infected human aortic endothelial cells.
Cellular microbiology. 8(5):738-57 [PMID] 16611224.
View on: PubMed
2006
Innate immune signaling and Porphyromonas gingivalis-accelerated atherosclerosis.
Journal of dental research. 85(2):106-21 [PMID] 16434728.
View on: PubMed
2006
Pathogen-accelerated atherosclerosis occurs early after exposure and can be prevented via immunization.
Infection and immunity. 74(2):1376-80 [PMID] 16428788.
View on: PubMed
2006
Roles of the host oxidative immune response and bacterial antioxidant rubrerythrin during Porphyromonas gingivalis infection.
PLoS pathogens. 2(7) [PMID] 16895445.
View on: PubMed
2006
The K1 serotype capsular polysaccharide of Porphyromonas gingivalis elicits chemokine production from murine macrophages that facilitates cell migration.
Infection and immunity. 74(11):6236-43 [PMID] 16940143.
View on: PubMed
2005
Sensitization of human aortic endothelial cells to lipopolysaccharide via regulation of Toll-like receptor 4 by bacterial fimbria-dependent invasion.
Infection and immunity. 73(12):8050-9 [PMID] 16299299.
View on: PubMed
2005
Porphyromonas gingivalis fimbria-dependent activation of inflammatory genes in human aortic endothelial cells.
Infection and immunity. 73(9):5367-78 [PMID] 16113252.
View on: PubMed
2005
Gingipain-specific IgG in the sera of patients with periodontal disease is necessary for opsonophagocytosis of Porphyromonas gingivalis.
Journal of periodontology. 76(10):1629-36 [PMID] 16253083.
View on: PubMed
2005
Inducible nitric oxide synthase mediates bone development and P. gingivalis-induced alveolar bone loss.
Bone. 36(3):472-9 [PMID] 15777672.
View on: PubMed
2004
Innate immune recognition of invasive bacteria accelerates atherosclerosis in apolipoprotein E-deficient mice.
Circulation. 109(22):2801-6 [PMID] 15123526.
View on: PubMed
2004
Porphyromonas gingivalis-specific immunoglobulin G prevents P. gingivalis-elicited oral bone loss in a murine model.
Infection and immunity. 72(4):2408-11 [PMID] 15039370.
View on: PubMed
2003
Immunization with Porphyromonas gingivalis capsular polysaccharide prevents P. gingivalis-elicited oral bone loss in a murine model.
Infection and immunity. 71(4):2283-7 [PMID] 12654858.
View on: PubMed
2003
Mice lacking inducible nitric oxide synthase demonstrate impaired killing of Porphyromonas gingivalis.
Infection and immunity. 71(9):4917-24 [PMID] 12933833.
View on: PubMed
2002
Fimbria-dependent activation of cell adhesion molecule expression in Porphyromonas gingivalis-infected endothelial cells.
Infection and immunity. 70(1):257-67 [PMID] 11748191.
View on: PubMed
2002
Role for fimbriae and lysine-specific cysteine proteinase gingipain K in expression of interleukin-8 and monocyte chemoattractant protein in Porphyromonas gingivalis-infected endothelial cells.
Infection and immunity. 70(1):268-76 [PMID] 11748192.
View on: PubMed
2001
Prevention of Porphyromonas gingivalis-induced oral bone loss following immunization with gingipain R1.
Infection and immunity. 69(12):7959-63 [PMID] 11705986.
View on: PubMed

Grants

Apr 2019 ACTIVE
Effect of SutroVax cocktail to prevent Porphyromonas gingivalis-elicited oral bone loss-efficacy #2
Role: Principal Investigator
Funding: VAXCYTE
Apr 2018 – Dec 2018
Molecular analysis of Porphyromonas
Role: Principal Investigator
Funding: VAXCYTE
Aug 2016 – Jun 2019
PPARs and periodontal disease
Role: Principal Investigator
Funding: NATL INST OF HLTH NIDCR
Sep 2015 ACTIVE
Regulatory Mechanisms Controlling Expression of P. gingivalis Surface Structures
Role: Co-Investigator
Funding: NATL INST OF HLTH NIDCR

Education

Ph.D. – Microbiology
1994 · University of New Hampshire
B.S. – Biology
1989 · University of New Hampshire

Teaching Profile

Courses Taught
2020-2021
DEN6421C Perio Tx Plan
2017,2020
DEN6128 Host Defense
2019-2020
DEN5127 Infectious Diseases
2018
GMS7980 Research for Doctoral Dissertation
2018
BMS6300 Fund Micro and Immuno

Contact Details

Phones:
Business:
(352) 273-8856
Emails: