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Eric Triplett

Eric Triplett

· Microbiology and Cell Science, University of FloridaVerified

University of Florida · Microbiology and Cell Science

Active 1974–2026

h-index82
Citations23.5k
Papers33277 last 5y
Funding$3.4M
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About

Professor Eric Triplett serves as Professor and Chair in the Department of Microbiology and Cell Science at the University of Florida. The overall goal of the Triplett lab is to determine the drivers of microbial diversity in a wide range of environments. This research focus highlights his commitment to understanding the factors that influence microbial communities, which is fundamental to advancing knowledge in microbiology and related fields.

Research topics

  • Medicine
  • Immunology
  • Environmental health
  • Genetics
  • Sociology
  • Biology
  • Computational biology
  • Bioinformatics
  • Endocrinology
  • Pediatrics
  • Medical education
  • Mathematics education
  • Physics
  • Psychology
  • Internal medicine

Selected publications

  • The inflammatory path toward type 1 diabetes begins during pregnancy

    Nature Communications · 2026-01-07 · 2 citations

    articleOpen access

    Type 1 diabetes (T1D) is increasing globally, yet the earliest biological determinants remain poorly defined, particularly in general population studies. We studied the Swedish population-based ABIS birth cohort (n = 16,683) to identify early-life risk factors. Olink proteomic analysis (n = 286 controls, n = 146 cases) of inflammatory signals at birth shows differential abundance years before diagnosis (mean age 12.6 years), with proteins enriched for neutrophil migration, cytotoxicity, extracellular matrix remodeling, and immune regulation. Several markers remain significant in spite of prenatal and perinatal factors including family history of diabetes, and are associated with differences in compounds like stearic acid, lysine, glutamine, and persistent, environmental toxicants perfluorodecylethanoic acid and perfluorooctane sulfonate (PFOS). Using machine learning, we identify a protein subset that predicts T1D with high accuracy (AUC = 0.89 ± 0.02), independently of HLA genetic risk. These findings suggest that innate and tissue-remodeling pathways are perturbed at birth, possibly reflecting early β-cell vulnerability. Identifying these disruptions at birth with a non-invasive method opens a window for prevention, protecting β-cells before the inflammatory attack on islets begins.

  • Structure and Spatial Heterogeneity of Chemosynthesis‐Based Deep‐Sea Archaeal and Bacterial Communities in Western South Atlantic

    Ecology and Evolution · 2026-02-01

    articleOpen access

    ABSTRACT Cold seeps are widespread deep‐sea ecosystems sustained by methane‐rich fluid seepage and host dense chemosynthesis‐based biological communities. In 2016, a methane‐driven chemosynthetic system was discovered on the Rio Grande Cone, in the Western South Atlantic Ocean, but the structure and drivers of its prokaryotic communities remained poorly understood. Here, we investigated archaeal and bacterial communities associated with deep‐sea sediments across three geographic areas (A, C, and E) and a vertical gradient of up to 18 m below the seafloor, encompassing sediment layers within and below the sulfate–methane transition zone (SMTZ). Community composition was assessed using high‐throughput sequencing of the 16S rRNA gene (V3‐V4 region), processed into amplicon sequence variants (ASVs), and related to local geochemical gradients using multivariate analyses. To disentangle the ecological responses of methane‐cycling taxa from the broader microbiome, the prokaryotic community was analyzed by contrasting the ANME‐SRB consortium with the remaining archaeal and bacterial taxa. Both groups exhibited significant spatial structuring across areas and sediment layers. Methane concentration and depth were the dominant drivers shaping both ANME‐SRB and the remaining prokaryotic community, with conductivity further influencing the latter. Core microbiome analysis revealed a small number of widespread taxa accounting for a large proportion of total community abundance, including an atypical dominance of the archaeal genus Sulfophobococcus . Functional predictions indicated a predominance of sulfur‐ and nitrogen‐related metabolisms, with no clear depth‐structured metabolic profiles across the SMTZ. Overall, our results highlight how local geochemical gradients shape both methane‐cycling and non‐methane‐cycling prokaryotic assemblages in a poorly explored South Atlantic cold seep, providing a baseline for future genome‐resolved investigations of microbial functioning in this system.

  • A case-cohort longitudinal study for the analysis of microbial associations and viruses on the risk of celiac disease (MAVRiC)

    medRxiv · 2025-05-27

    preprintOpen access

    Celiac disease etiopathogenesis requires genetic predisposition and exposure to gluten before a child can develop the chronic autoimmune disorder. However, these factors alone are not sufficient. Even a child with persistent tissue transglutaminase autoantibodies (tTGA), i.e., celiac disease autoimmunity (CDA), does not necessarily develop celiac disease. Larger longitudinal studies are needed to determine the impact of time-varying infections and gut microorganisms on the subsequent and specific risk of celiac disease. The aim was to design a celiac disease case-cohort longitudinal study using The Environmental Determinants of Diabetes in the Young (TEDDY) study. Following the TEDDY cohort up age 3-years, CDA was confirmed in 704 of the 6132 genetically at-risk children. Celiac disease onset was defined as the age CDA developed when followed by a biopsy-proven diagnosis. A competing risk analysis was performed on celiac disease onset cases (CD-onset) as well as CDA children with no diagnosis (CDA-only) and results show genetic factors (additional HLA-DR3-DQ2 haplotype, higher non-HLA polygenic risk score, sex-girl) and a more rapid increase in gluten-consumption correlate with significant increased risk of both outcomes. However, reports of virus-related respiratory infections in August to October during follow-up correlated with an increased risk of a CD-onset but not with CDA-only. To create a case-cohort study, a sub-cohort of 561 children (9% sampling fraction) was first randomly selected to represent the TEDDY cohort over time while at risk of CDA. It included 483 children followed until age 3-years and 78 children followed before developing CDA (CDA-only n=41/78, CD-onset n=37/78). All incident CD-onset children (N=306) were included to form the case group. This case-cohort will be utilized to analyze virus antibodies and bacteriome from longitudinal plasma and stool samples (the Microbial Associations and Viruses on the Risk of Celiac disease study, MAVRiC).

  • Microbial associations and viruses on the risk of celiac disease (MAVRiC): a longitudinal post-hoc case-cohort study

    Scientific Reports · 2025-11-28

    articleOpen access

    Celiac disease etiopathogenesis requires genetic predisposition and exposure to gluten, yet these factors alone are not sufficient. Larger longitudinal studies are needed to determine the role of time-varying infections and gut microorganisms. The aim was to design a celiac disease case-cohort longitudinal study using The Environmental Determinants of Diabetes in the Young (TEDDY) study. By age 3-years, persistent tissue transglutaminase autoantibodies (tTGA), i.e., celiac disease autoimmunity (CDA), was confirmed in 704 of the 6132 genetically at-risk TEDDY children. Celiac disease onset (CD-onset) was defined as the age CDA developed when followed by a biopsy-proven diagnosis. A competing risk analysis on CD-onset and CDA children with no diagnosis (CDA-only) revealed female-sex, HLA and non-HLA genes and higher gluten-consumption correlate with an increased risk of both outcomes. However, reports of virus-related respiratory infections from August to October correlate consistently with an increased risk of CD-onset and not CDA-only. A sub-cohort of 561 children (9% sampling fraction) has been randomly selected to represent the TEDDY cohort. All incident CD-onset cases (N = 306) were included. The case-cohort will be utilized to analyze virus antibodies and bacteriome from longitudinal plasma and stool samples (the Microbial Associations and Viruses on the Risk of Celiac disease study, MAVRiC).

  • Unfolding the Mystery of Autoimmunity: The Environmental Determinants of Diabetes in the Young (TEDDY) Study

    Diabetes Care · 2025-04-24 · 7 citations

    reviewOpen access

    In 2025, the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) at the National Institutes of Health celebrates 75 years of leadership in diabetes research. The NIDDK serves people of the U.S. affected by or at risk for many chronic diseases, including diabetes and other endocrine, metabolic, and digestive disorders, by funding innovative research to develop better treatment and prevention and a cure for these conditions. Autoimmunity that leads to type 1 diabetes or celiac disease or thyroid autoimmunity affects 1 in 20 children and adolescents in the U.S. While treatments are available, prevention of these common autoimmune diseases has been elusive due to poor understanding of the environmental causes and their interactions with common predisposing or protective genetic variants. In 2002, the NIDDK established The Environmental Determinants of Diabetes in the Young (TEDDY) consortium to advance understanding of the causes and the natural history of type 1 diabetes and other autoimmune diseases. The overarching goal of TEDDY is to inform novel approaches to primary prevention of autoimmunity. In this large international prospective birth cohort study, standardized information has been collected concerning candidate environmental exposures along with serial blood, stool, nasal swab, and other biosamples, with creation of a central repository of data and biologic samples for hypothesis-based research. This review summarizes TEDDY's major contributions to our understanding of environmental triggers, drivers, and modifiers of autoimmunity, and gene-environment interactions, leading to type 1 diabetes.

  • Unfolding the Mystery of Autoimmunity: The Environmental Determinants of Diabetes in the Young (TEDDY) Study

    2025-04-24

    preprintOpen access

    <p dir="ltr">In 2025, the National Institute for Diabetes, Digestive and Kidney Diseases (NIDDK) at the National Institutes of Health celebrates 75 years of leadership in diabetes research. The NIDDK serves people of the United States affected by or at risk for many chronic diseases, including diabetes and other endocrine, metabolic and digestive disorders by funding innovative research to develop better treatment, prevention, and cure for these conditions. Autoimmunity that leads to type 1 diabetes, celiac or thyroid autoimmunity affects one in twenty children and adolescents in the USA. While treatments are available, prevention of these common autoimmune diseases has been elusive due to poor understanding of the environmental causes and their interactions with common predisposing or protective genetic variants.</p><p dir="ltr">In 2002, the NIDDK established The Environmental Determinants of Diabetes in the Young (TEDDY) consortium to advance understanding of the causes and the natural history of type 1 diabetes and other autoimmune diseases. The overarching goal of TEDDY is to inform novel approaches to primary prevention of autoimmunity. This large international prospective birth cohort study has collected standardized information concerning candidate environmental exposures and serial blood, stool, nasal swab and other biosamples and created a central repository of data and biologic samples for hypothesis-based research. This review summarizes TEDDY’s major contributions to our understanding of environmental triggers, drivers, modifiers, and gene-environment interactions leading to type 1 diabetes.</p>

  • Effect of a Mediterranean-Style Diet Educational Intervention on Symptoms of Depression, Anxiety, and Stress in College Students: A Randomized Trial

    Current Developments in Nutrition · 2025-05-01

    articleOpen accessSenior author
  • Risk Evaluation and Molecular Characterisation of <scp> <i>AtNPR1</i> </scp> Transgenic Citrus Lines Tolerant to Citrus Greening Disease

    Plant Biotechnology Journal · 2025-10-13

    articleOpen accessCorresponding

    Citrus greening disease, or Huanglongbing (HLB), has caused devastating losses to citrus production in Florida, with yields declining by over 90% since 2005. Despite extensive efforts, no sustainable solution has been widely effective. Here, transgenic 'Hamlin' sweet orange lines engineered to constitutively express the Arabidopsis NPR1 (AtNPR1) gene, a key regulator of systemic acquired resistance, are evaluated for health and environmental risks. These citrus lines exhibit strong HLB tolerance, with reduced disease symptoms, sustained fruit production, and no apparent negative phenotypic abnormalities. Comprehensive risk assessment reveals minimal exposure, health, or environmental risk. The AtNPR1 protein is: (1) barely detectable in fruit, (2) rapidly degraded in simulated gastrointestinal fluids, and (3) not similar to known allergens or toxins. Whole-genome sequencing identified the T-DNA insertion sites as heterozygous in either chromosome 1 or 6, with no disruptions in known fruit-producing genes. PCR markers were developed for rapid line identification. The selected lines are currently in a small field trial under high HLB pressure and continue to exhibit low visual HLB symptoms and positive horticultural traits. These findings support the initial requirements for regulatory approval of these transgenic citrus varieties, offering a promising strategy for sustainable citrus production.

  • Unfolding the Mystery of Autoimmunity: The Environmental Determinants of Diabetes in the Young (TEDDY) Study

    2025-04-24

    preprintOpen access

    &lt;p dir="ltr"&gt;In 2025, the National Institute for Diabetes, Digestive and Kidney Diseases (NIDDK) at the National Institutes of Health celebrates 75 years of leadership in diabetes research. The NIDDK serves people of the United States affected by or at risk for many chronic diseases, including diabetes and other endocrine, metabolic and digestive disorders by funding innovative research to develop better treatment, prevention, and cure for these conditions. Autoimmunity that leads to type 1 diabetes, celiac or thyroid autoimmunity affects one in twenty children and adolescents in the USA. While treatments are available, prevention of these common autoimmune diseases has been elusive due to poor understanding of the environmental causes and their interactions with common predisposing or protective genetic variants.&lt;/p&gt;&lt;p dir="ltr"&gt;In 2002, the NIDDK established The Environmental Determinants of Diabetes in the Young (TEDDY) consortium to advance understanding of the causes and the natural history of type 1 diabetes and other autoimmune diseases. The overarching goal of TEDDY is to inform novel approaches to primary prevention of autoimmunity. This large international prospective birth cohort study has collected standardized information concerning candidate environmental exposures and serial blood, stool, nasal swab and other biosamples and created a central repository of data and biologic samples for hypothesis-based research. This review summarizes TEDDY’s major contributions to our understanding of environmental triggers, drivers, modifiers, and gene-environment interactions leading to type 1 diabetes.&lt;/p&gt;

  • Temporal dynamics of the gut microbiome preceding celiac disease in genetically at-risk children

    medRxiv · 2025-05-31

    preprintOpen accessCorresponding

    Abstract Longitudinal study of the microbial dysbiosis preceding celiac disease (CD) is needed, particularly in the first several years of life. Within the Environmental Determinants of Diabetes in the Young (TEDDY) multi-national prospective cohort study, a case-cohort study of 306 CD cases (i.e., seroconverting by 48 months of age), with controls matched 2:1 by site, gender, and time of birth, was assessed. Temporal microbiome case-control dynamics were modelled by 16S rRNA analysis of monthly sequential stool samples taken from age three months up to age four (or until the development of CD). Significant differences were identified across time, including key taxa that break down gluten and influence inflammation, all before the development of autoantibodies. Key bacterial associations with environmental factors such as diet were assessed using detailed longitudinal nutrient intake and diary data, along with genetic variants conferring high CD risk.

Recent grants

Frequent coauthors

  • Åke Lernmark

    77 shared
  • Desmond Schatz

    University of Florida

    74 shared
  • Jorma Toppari

    Copenhagen University Hospital

    71 shared
  • William Hagopian

    University of Washington

    63 shared
  • Anette G. Ziegler

    57 shared
  • Helena Elding Larsson

    Lund University

    55 shared
  • Beena Akolkar

    National Institute of Diabetes and Digestive and Kidney Diseases

    54 shared
  • Sandra Hummel

    German Center for Diabetes Research

    54 shared

Awards & honors

  • 2021 American Society for Microbiology William A. Hinton Awa…
  • 2020 Elected Fellow of the American Association for the Adva…
  • 2019 Association of Public & Land-Grant Universities Academi…
  • 2019 University of Missouri CAFNR Alumni Columns Award
  • 2011 American Society for Microbiology International Profess…
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