星空无限传媒

星空无限传媒
星空无限传媒 星空无限传媒
Research Bench Lab
Microbiology & Immunology
Jenifer Coburn, PhD

Jenifer Coburn, PhD

Professor, Medicine (Infectious Diseases) and Microbiology & Immunology; Center for Infectious Disease Research

Locations

  • Center for Infectious Disease Research
    TBRC C3980

Contact Information

General Interests

Bacterial Pathogenesis

Education

PhD, Molecular Microbiology, Tufts University, 1991

Research Experience

  • Borrelia Infections
  • Spirochaetales Infections
  • Tick-Borne Diseases

Research Interests

Coburn Lab Group Shot

Research interests focus on pathogenic spirochetes, a group of bacteria that are able to cause persistent, disseminated infections in immunocompetent animals, including humans. We are currently working with Borrelia burgdorferi, which is maintained in a tick-animal cycle in nature. We also work with another pathogenic spirochete, Leptospira interrogans. Leptospires are maintained in infected animals in nature, but can also survive in water and mud. The focus of our work with both Borrelia and Leptospira is to identify and then test the biologic significance of bacterial proteins that help the bacteria bind to mammalian cell surface receptors, to identify the mammalian cell surface receptors recognized by the bacteria, and ultimately the biological and pathologic significance of the bacterial-mammalian receptor interaction.

In the Borrelia work, we have two main projects ongoing in the lab. In one, we are trying to understand the mechanisms behind the requirement for the B. burgdorferi protein, P66, for the bacteria to cause infection in mammals. P66 binds to mammalian cell surface receptors called integrins and serves as a porin in the bacterial outer membrane. We know that the integrin binding function is important for the bacteria to cross endothelial layers and disseminate to different sites in the body. In another Borrelia project, we developed a new experimental model to determine the roles of bacterial adhesive proteins in how the bacteria colonize different tissues in mammals, and how they survive the mammalian defenses in the bloodstream.

coburn_figure1

Figure 1. This image is an Ixodes scapularis tick. Shown is the nymphal stage of the tick; the scale bar is 1 mm so these ticks are tiny. These ticks are important in transmitting Borrelia burgdorferi to new host animals, and sometimes to humans.

coburn_figure2

Figure 2: B. burgdorferi producing a red fluorescent protein in a dispersed tick midgut.

In the Leptospira work, we also focus in how the bacteria interact with endothelial cells. In severe cases of leptospirosis, widespread endothelial damage is seen, and this is associated with hemorrhage. L. interrogans binds to an endothelial cell surface receptor called VE-cadherin, which helps the endothelial cells form cell-cell junctions that maintain the integrity of small blood vessels. We are currently determining how the bacteria disrupt cadherin-cadherin interactions, and determining whether the bacterial proteins that bind VE-cadherin are responsible for the endothelial disruption caused by the bacteria. In a second Leptospira project, we are working to identify the bacterial proteins that help the bacteria bind to kidney cells, as the kidneys are where the bacteria reside in a chronically infected animal and from where they are released into the environment.

coburn_figure3

Figure 3: Leptospira interrogans (red) binding to human endothelial cells. An endothelial cell surface receptor for L. interrogans, VE-cadherin, is stained in green, but the cell-cell junctions are mostly disrupted. The endothelial cell nuclei are stained in blue.

Publications

  • (Tal MC, Hansen PS, Ogasawara HA, Feng Q, Volk RF, Lee B, Casebeer SE, Blacker GS, Shoham M, Galloway SD, Sapiro AL, Hayes B, Torrez Dulgeroff LB, Raveh T, Pothineni VR, Potula HS, Rajadas J, Bastounis EE, Chou S, Robinson WH, Coburn J, Weissman IL, Zaro BW.) bioRxiv. 2024 Apr 30 PMID: 38746193 PMCID: PMC11092639 05/15/2024

  • (Tan X, Lin YP, Pereira MJ, Castellanos M, Hahn BL, Anderson P, Coburn J, Leong JM, Chaconas G.) PLoS Pathog. 2022 May;18(5):e1010511 PMID: 35605029 PMCID: PMC9166660 SCOPUS ID: 2-s2.0-85131457166 05/24/2022

  • (Curtis MW, Fierros CH, Hahn BL, Surdel MC, Kessler J, Anderson PN, Vandewalle-Capo M, Bonde M, Zhu J, Bergström S, Coburn J.) Front Cell Infect Microbiol. 2022;12:991689 PMID: 36211976 PMCID: PMC9539438 SCOPUS ID: 2-s2.0-85139437187 10/11/2022

  • (Surdel MC, Hahn BL, Anderson PN, Coburn J.) Front Cell Infect Microbiol. 2022;12:917963 PMID: 35937702 PMCID: PMC9354625 SCOPUS ID: 2-s2.0-85135274644 08/09/2022

  • (Surdel MC, Anderson PN, Hahn BL, Coburn J.) Front Cell Infect Microbiol. 2022;12:917962 PMID: 35923802 PMCID: PMC9339599 SCOPUS ID: 2-s2.0-85135250975 08/05/2022

  • (Coburn J, Picardeau M, Woods CW, Veldman T, Haake DA.) PLoS Pathog. 2021 Oct;17(10):e1009836 PMID: 34673833 PMCID: PMC8530280 SCOPUS ID: 2-s2.0-85118294631 10/22/2021

  • (Coburn J, Garcia B, Hu LT, Jewett MW, Kraiczy P, Norris SJ, Skare J.) Curr Issues Mol Biol. 2021;42:473-518 PMID: 33353871 PMCID: PMC8046170 SCOPUS ID: 2-s2.0-85102523563 12/24/2020

  • (Hahn B, Anderson P, Lu Z, Danner R, Zhou Z, Hyun N, Gao L, Lin T, Norris SJ, Coburn J.) Microbiology (Reading). 2020 Oct;166(10):988-994 PMID: 32936070 PMCID: PMC7660918 SCOPUS ID: 2-s2.0-85094983555 09/17/2020

  • (DeCero SA 2nd, Winslow CH, Coburn J.) J Biomol Tech. 2020 Sep;31(3):94-99 PMID: 32831656 PMCID: PMC7351327 SCOPUS ID: 2-s2.0-85091559248 08/25/2020

  • (Lin YP, Tan X, Caine JA, Castellanos M, Chaconas G, Coburn J, Leong JM.) PLoS Pathog. 2020 May;16(5):e1008516 PMID: 32413091 PMCID: PMC7255614 SCOPUS ID: 2-s2.0-85085664567 05/16/2020

  • (Eshghi A, Gaultney RA, England P, Brûlé S, Miras I, Sato H, Coburn J, Bellalou J, Moriarty TJ, Haouz A, Picardeau M.) Cell Microbiol. 2019 Feb;21(2):e12949 PMID: 30171791 PMCID: PMC7560960 SCOPUS ID: 2-s2.0-85053836084 09/02/2018

  • (Winslow C, Coburn J.) F1000Res. 2019;8 PMID: 31214329 PMCID: PMC6545822 SCOPUS ID: 2-s2.0-85067361276 06/20/2019

Publications of from the