Richard J. Lamont, PhD

Richard J. Lamont, PhD

Richard J. Lamont

Delta Dental Endowed Professor
Chair, Oral Immunology and Infectious Diseases
Room 221B, Baxter I
Phone: 502 852 2112

Research Interests:

The oral cavity is a complex ecosystem that is home to a diverse assemblage of bacteria with a spectrum of pathogenic potentials.  On tooth surfaces these organisms assemble into a complex multispecies biofilm community, commonly known as dental plaque.  Community formation is a dynamic process involving attachment of bacteria to oral surfaces, cohesion and communication among constituent organisms, and adaptation to the biofilm environment.  The composition and metabolic status of the resulting community determines whether the biofilm exists in commensal harmony with the host, or becomes a precursor to caries and periodontal disease, two of the most common bacterial diseases of humans.

Major Projects

1.  Molecular and cellular dialog between Porphyromonas gingivalis and gingival epithelial cells (GECs). 

 In the latter decades of the 20th century the scientific community began to appreciate that epithelial cells are not simply a passive barrier to microbial intrusion, but rather constitute an interactive interface that can sense the presence of bacteria and signal their presence to underlying immune cells.  Colonizing bacteria, for their part, can subvert host cell signaling systems to direct their uptake into the otherwise non-professionally phagocytic epithelial cells, and to manipulate host cell physiology.  My group was among the first to show that P. gingivalisactively invades epithelial cells, which we established in a novel model system utilizing primary cultures of GECs.  Dissection of the molecular and cellular dialog between P. gingivalis and GECs then became a major research focus. We have found that internalization of P. gingivalis is effectuated by a limited number of functionally versatile invasins, including the FimA fimbriae and the serine phosphatase SerB, which impact cytoskeletal integrity and thus allow bacteria entry.  Co-habiting bacteria and GECs remain viable and adaptation of both cell types involves major changes in the transcriptome and expressed proteome.  Phenotypic consequences for the host cell include disruption of cytokine signaling along suppression of apoptotic cell death pathways, acceleration through the cell cycle and initiation of the epithelial-mesenchymal transition.  Collectively, this work defined a new aspect of the P. gingivalis-host interaction with relevance for homeostatic imbalance, long term P. gingivalis survival in the host, and recrudescence of infection.

Representative publications

  1. Ohshima J, Wang Q, Fitzsimonds ZR, Miller DP, Sztukowska NM, Jung Y-J, Hayashi M, Whiteley M, Lamont RJ. 2019. Streptococcus gordonii programs epithelial cells to resist ZEB2 induction by Porphyromonas gingivalis. Proc Natl Acad Sci USA 10.1073/pnas.1900101116
  2. Sztukowska MN, Ojo A, Ahmed S, Carenbauer AL, Wang Q, Shumway B, Jenkinson HF, Wang H, Darling DS, Lamont RJ. 2016.  Porphyromonas gingivalis initiates a mesenchymal-like transition through ZEB1 in gingival epithelial cells. Cell Microbiol 18:844-858. PMC5135094
  3. Wang Q, Sztukowska M, Ojo A, Scott DA, Lamont RJ, Wang H. 2015. FOXO responses to Porphyromonas gingivalis in epithelial cells. Cell Microbiol 17:1605-1617.  PMC4624012
  4. Takeuchi H, Hirano T, Whitmore SE, Morisakai I, Amano A, Lamont RJ. 2013. The serine phosphatase SerB of Porphyromonas gingivalis suppresses IL-8 production by dephosphorylation of NF-κB RelA/p65. PLoS Pathog 9:e1003326.  PMC3630210
  5. Moffatt CE, Inaba H, Hirano T, Lamont RJ.  2012.  Porphyromonas gingivalis SerB-mediated dephosphorylation of host cell cofilin modulates invasion efficiency. Cell Microbiol 14:577-588.  PMC3449298
  6. Tribble GD, Mao S, James CE, Lamont RJ. 2006. A Porphyromonas gingivalis haloacid dehalogenase family phosphatase interacts with human phosphoproteins and is important for invasion. Proc Natl Acad Sci U S A 103:11027-11032.


2.  P. gingivalis assembles into communities with antecedent colonizers
 Work from the Kolenbrander lab and others had shown that oral bacteria form interspecies networks of conglomorated organisms.  Landmark studies by Slots and Gibbons in the 1970s demonstrated that initial colonization of plaque by P. gingivalis requires attachment to antecedent streptococcal colonizers, and close association of P. gingivalis with streptococci has been corroborated by more recent imaging studies. We have defined P. gingivalis-S. gordonii interacting adhesinsand their functional domains.  Moreover, our group was among the pioneers of the field of sociomicrobiology: the investigation of the communication and synergy that occurs among groups of physiologically compatible organisms in communities.  We have defined chemical communication (based on AI-2) and contact dependent communication (based on a cascade of protein tyrosine phosphorylation and dephosphorylation events) between P. gingivalis and S. gordonii.  The importance of this interaction in vivo was demonstrated by our finding that communities of P. gingivalis and S. gordonii cause more alveolar bone loss in mice compared to infection with either species alone and moreover, inhibition of coadhesion prevents community-mediated bone loss.  Hence this work has identified additional targets for potential therapeutic intervention to inhibit P. gingivalis colonization and the transition of the plaque biofilm to a pathogenic entity. 

Representative publications

  1. Kuboniwa M, Houser JR, Hendrickson EL, Wang Q, Alghamdi SA, Sakanaka A, Miller DP, Hutcherson JA, Wang T, Beck DAC, Whiteley M, Amano A, Wang H, Marcotte EM, Hackett M, Lamont RJ. 2017.  Metabolic crosstalk regulates Porphyromonas gingivalis colonization and virulence during oral polymicrobial infection.  Nat Microbiol. 2: 1493-1499.  PMC5678995
  2. Wright CJ, Xue P, Hirano T, Liu C, Whitmore SE, Hackett M, Lamont RJ. 2014. Characterization of a bacterial tyrosine kinase in Porphyromonas gingivalis involved in polymicrobial synergy. MicrobiologyOpen 3:383-394. PMC4082711
  3. Chawla A, Hirano T, Bainbridge BW, Demuth DR, Xie H, Lamont RJ. 2010.  Community signalling between Streptococcus gordonii and Porphyromonas gingivalis is controlled by the transcriptional regulator CdhR.  Mol Microbiol 78:1510-1522.  PMC3017474
  4. Maeda K, Tribble GT, Tucker CM, Anaya C, Shizukuishi S, Lewis JP, Demuth DR, Lamont RJ. 2008. A Porphyromonas gingivalis tyrosine phosphatase is a multifunctional regulator of virulence attributes.  Mol Microbiol 69:1153-1164.  PMC2537464
  5. Daep CA, Novak EA, Lamont RJ, Demuth DR. 2011. Structural dissection and in vivo effectiveness of a peptide inhibitor of Porphyromonas gingivalis adherence to Streptococcus gordonii. Infect Immun.79:67-74.


3.  Formulating a new model of periodontal disease pathogenesis
 In collaboration with Dr. Hajishengallis, and to draw all the above concepts together in combination with Dr. Hajishengallis’ conceptual advances, we have proposed a theory of periodontal disease pathogenesis based on polymicrobial synergy and dysbiosis (PSD).  The PSD model holds that periodontal disease ensues from the action of a polymicrobial community in which pathogenicity is defined by interactions among functionally specialized organisms including keystone pathogens and accessory pathogens.  Pathogenic communities then induce dysbiotic host responses which fail to control the microbial challenge and contribute to tissue destruction.  The original paper describing the PSD model has been cited over 250 times since 2012.  We are currently pursuing testable predictions based on this model which we believe will significantly advance the field. 

  1. Lamont RJ, Koo H, Hajishengallis G, 2018 The oral microbiota: dynamic communities and host interaction.  Nature Microbiol 16:745-759.  PMC6278837
  2. Hajishengallis G, Lamont RJ. 2016. Dancing with the Stars: How Choreographed Bacterial Interactions Dictate Nososymbiocity and Give Rise to Keystone Pathogens, Accessory Pathogens, and Pathobionts. Trends Microbiol 24:477-489.   PMC4874887
  3. Lamont RJ, Hajishengallis G. 2015. Polymicrobial synergy and dysbiosis in inflammatory disease. Trends Mol Med 21: 172-183.   PMC4352384
  4. Hajishengallis G, Lamont RJ. 2014.  Breaking bad: manipulation of the host response by Porphyromonas gingivalis.  Eur J Immunol 44:328-338. PMC3925422
  5. Hajishengallis G, Lamont RJ. 2012. Beyond the red complex and into more complexity: the polymicrobial synergy and dysbiosis (PSD) model of periodontal disease etiology. Mol Oral Microbiol 27:409-419.  PMC3653317

Complete List of Published Work in MyBibliography