Jorge Frias-Lopez, Ph.D.
Department of Oral Biology
1395 Center Drive, DG-37
Gainesville, FL, 32610-0424
- Ph. D. Microbiology, University of Barcelona. Spain, 1992
- B.Sc. Biology, University of Barcelona. Spain, 1987
- Forsyth Institute, Associate Member of the Staff 2013-2016
- Forsyth Institute, Assistant Member of the Staff 2010-2013
- Forsyth Institute, Assistant Research Investigator 2008-2010
- Harvard School of Dental Medicine, Lecturer 2008-2016
- Massachusetts Institute of Technology, Research Scientist 2004-2008
- University of Illinois Urbana-Champaign, Postdoctoral Research Associate 2001-2004
My research interests are concentrated on studying the ecology of the human microbiome focusing on the oral microbial community. Quoting the overview section of the Human Microbiome Project: “Within the body of a healthy adult, microbial cells are estimated to outnumber human cells ten to one. This community, however, remains largely unstudied, leaving their influence upon human development, physiology, immunity, and nutrition almost entirely unknown”. This lack of knowledge is what makes this field of such importance. Within this context, I use oral polymicrobial diseases (periodontal disease) as a model to study and understand complex human microbial communities and the interactions among their members and with their host.
The unifying theme of my work is to understand the role that microbial communities play in human health and disease.
Working at MIT I developed a set of tools that facilitate the study of gene expression in whole microbial communities (metatranscriptome) and not just in one specific organism (Frias-Lopez et al. 2008, Microbial community gene expression in ocean surface waters).
Currently, the main focus of my research is understanding the mechanisms of progression of the most common infectious polymicrobial inflammatory disease: periodontal disease. I have been awarded with an R01 grant from NIH to study changes in the metagenome and metatranscriptome of the oral community that could explain why in some cases disease progresses and in other it does not.
Current and Future Research
- Gene expression of the human microbiome in health and disease.
Periodontitis is a polymicrobial biofilm-induced inflammatory disease that occurs in moderate form in 30% to 50% of American adults and in severe form in 10% of adults and it is responsible for half of all tooth loss in adults. It is the sixth most prevalent health condition in the world affecting 743 million people worldwide. The total expenditure on treating and preventing periodontal diseases was estimated at $14B in the United States. In addition, recent studies have suggested that periodontal diseases can influence the risk for certain systemic conditions such as cardiovascular diseases, diabetes, respiratory diseases, and can affect reproductive outcome. One main focus in my lab is using metatranscriptomic analysis to identify in situ genes that are differentially expressed in complex microbial communities in health and disease, specifically studying differences in gene expression of progressing and non-progressing periodontal sites to understand what causes the progression of the disease only in specific sites but not in others.
- How human microbial communities are structured: The role of keystone species and the study of stability.
Another of my research interests is trying to understand how oral microbial communities are structured and what are the driving forces that shape them. Using system biology approaches (weighted correlation network analysis) we have identified bacterial modules in the pathogenic microbial community that were associated with disease. The use of these techniques facilitates the understanding of such a complex community as the oral microbial community. More importantly, within these modules we were able to single out organisms with high centrality (‘keystone’) within those modules. These organisms could act as ‘keystone’ species in the community. To test our hypothesis we have started a series of experiments using some of those modules as a model and looking at the effect of the presence/absence of the ‘keystone’ species on biofilm integrity.
Linked to the overall theme of the structure of microbial communities is my interest on understanding what makes a community resilient to environmental changes and how to quantify the robustness of microbial communities. As a part of our current reseach on disease progression we study samples from diseased individuals after treatment. The study of these samples will allow us to get insights on what constitute a healthy steady-state community: would the community return to the same composition observed in healthy sites from the same individual or it is the patterns of gene expression what defines health and after treatment we achieve a different healthy steady-state composition to similar activities to healthy sites?
- The oral microbiome and cancer.
We have recently started a collaborative project, with Dr. Maria A. Kukuruzinska at Boston University and the Dana-Farber Cancer Institute in Boston, to study the potential role that the oral microbiome plays in oral cancer, charaterizing the profiles of gene expression of the microbial communities colonizing active cancer sites by metatranscriptome analysis as well as of the host response on those sites.
Frias-Lopez J. 2015. Targeting specific bacteria in the oral microbiome. Trends Microbiol. 23(9):527-8.
Duran-Pinedo AE, Yost S, Frias-Lopez J. 2015. Small RNA Transcriptome of the Oral Microbiome during Periodontitis Progression. Appl Environ Microbiol. 81(19):6688-99.
Yost S, Duran-Pinedo AE, Teles R, Krishnan K, Frias-Lopez J. 2015. Functional signatures of oral dysbiosis during periodontitis progression revealed by microbial metatranscriptome analysis. Genome Medicine. 7:(1)27.
Duran-Pinedo AE Frias-Lopez J. 2015. Beyond microbial community composition: functional activities of the oral microbiome in health and disease. Microbes and Infection. 17(7):505-16.
Duran-Pinedo AE, Chen T, Teles R, Starr JR, Wang X, Krishnan K, Frias-Lopez J. 2014. Community-wide transcriptome of the oral microbiome in subjects with and without periodontitis. ISME J. 8(8):1659-72.
Duran-Pinedo AE, Baker VD, Frias-Lopez J. 2014. The periodontal pathogen Porphyromonas gingivalis induces expression of transposases and cell death of Streptococcus mitis in a biofilm model. Infect Immun. 82(8):3374-82.
Diaz PI, Hong BY, Frias-Lopez J, Dupuy AK, Angeloni M, Abusleme L, Terzi E, Ioannidou E, Strausbaugh LD, Dongari-Bagtzoglou A. 2013. Transplantation-associated long-termimmunosuppression promotes oral colonization by potentially opportunistic pathogens without impacting other members of the salivary bacteriome. Clin Vaccine Immunol. 20(6):920-930.
Teles R, Teles F, Frias-Lopez J, Paster B, Haffajee A. 2013. Lessons learned and unlearned in periodontal microbiology. Periodontology 2000. 62(1):95-162.
Frias-Lopez J, Duran-Pinedo A. 2012. Effect of periodontal pathogens on the metatranscriptome of a healthy multispecies biofilm model. J Bacteriol. vol. 194 no. 8 2082-2095
Duran-Pinedo AE, Paster B, Teles R, Frias-Lopez J. 2011. Correlation network analysis applied to complex biofilm communities. PLoS One. 2011;6(12):e28438.
Malmstrom RR, Coe A, Kettler GC, Martiny AC, Frias-Lopez J, Zinser ER, Chisholm SW. 2010 Temporal dynamics of Prochlorococcus ecotypes in the Atlantic and Pacific oceans. ISME J. 4(10):1252-64. Epub 2010 May 13.
Osburne MS, Holmbeck BM, Frias-Lopez J, Steen R, Huang K, Engelking J, Chisholm SW. 2010. A UV-resistant Prochlorococcus marinus MED4 mutant overexpresses photoreactivation genes. Environ. Microbiol. 12(7):1978-88. Epub 2010 Mar 23.
J.Frias-Lopez, A. Thompson, J. Waldbauer & S.W. Chisholm. 2009. Use of stable isotope-labeled cells to identify active grazers of picocyanobacteria in ocean surface waters. Environmental Microbiology. 11:512-525.
J.Frias-Lopez, Y. Shin, G. Tyson, M. Coleman, S.W. Chisholm, & E. F. DeLong. 2008. Microbial gene expression in the surface oceans. PNAS.105:3805-3810