Beverly Koller

About

Beverly Koller is an Associate Professor at the University of North Carolina School of Medicine, specializing in the use of gene targeting techniques to create animal mouse models for human diseases and to identify genes that modify disease progression. Her research involves introducing specific genetic modifications into the genomes of experimental animals through homologous recombination and embryonic stem (ES) cell technology. This approach allows her to generate chimeric animals and, through germ line transmission, establish mouse lines carrying desired mutations for in vivo study. Her laboratory has utilized gene targeting to develop an animal model for cystic fibrosis, the most common genetic disease in the Caucasian population, and continues to refine this model to better resemble the human condition. Additionally, her research focuses on the study of inflammatory processes involved in allergic responses, asthma, and arthritis. Her team aims to generate animals deficient in various factors believed to be important in these diseases, with the goal of gaining a better understanding of the immunological processes underlying these conditions and identifying more effective treatments.

Research topics

• Biology
• Genetics
• Immunology
• Medicine
• Virology
• Cell biology

Selected publications

• Dual vaccination against IL-4 and IL-13 protects against chronic allergic asthma in mice

  Nature Communications · 2021 · 121 citations

  Allergic asthma is characterized by elevated levels of IgE antibodies, type 2 cytokines such as interleukin-4 (IL-4) and IL-13, airway hyperresponsiveness (AHR), mucus hypersecretion and eosinophilia. Approved therapeutic monoclonal antibodies targeting IgE or IL-4/IL-13 reduce asthma symptoms but require costly lifelong administrations. Here, we develop conjugate vaccines against mouse IL-4 and IL-13, and demonstrate their prophylactic and therapeutic efficacy in reducing IgE levels, AHR, eosin…

  PublisherOA PDFDOI

• Initiator cell death event induced by SARS-CoV-2 in the human airway epithelium

  Science Immunology · 2024-07-12 · 40 citations

  articleOpen access

  Virus-induced cell death is a key contributor to COVID-19 pathology. Cell death induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is well studied in myeloid cells but less in its primary host cell type, angiotensin-converting enzyme 2 (ACE2)-expressing human airway epithelia (HAE). SARS-CoV-2 induces apoptosis, necroptosis, and pyroptosis in HAE organotypic cultures. Single-cell and limiting-dilution analysis revealed that necroptosis is the primary cell death event in infe…

  PublisherOA PDFDOI

• Arsenic Metabolism in Mice Carrying a <i>BORCS7/AS3MT</i> Locus Humanized by Syntenic Replacement

  Environmental Health Perspectives · 2020 · 38 citations

  1st authorCorresponding

  BACKGROUND: Chronic exposure to inorganic arsenic (iAs) is a significant public health problem. Methylation of iAs by arsenic methyltransferase (AS3MT) controls iAs detoxification and modifies risks of iAs-induced diseases. Mechanisms underlying these diseases have been extensively studied using animal models. However, substantive differences between humans and laboratory animals in efficiency of iAs methylation have hindered the translational potential of the laboratory studies. OBJECTIVES: gen…

  DOI

• Species-specific NLRP3 regulation and its role in CNS autoinflammatory diseases

  Cell Reports · 2024-02-29 · 21 citations

  articleOpen access1st authorCorresponding

  The NLRP3 inflammasome is essential for caspase-1 activation and the release of interleukin (IL)-1β, IL-18, and gasdermin-D in myeloid cells. However, research on species-specific NLRP3's physiological impact is limited. We engineer mice with the human NLRP3 gene, driven by either the human or mouse promoter, via syntenic replacement at the mouse Nlrp3 locus. Both promoters facilitate hNLRP3 expression in myeloid cells, but the mouse promoter responds more robustly to LPS. Investigating the dise…

  PublisherOA PDFDOI

• Human ACE2 expression, a major tropism determinant for SARS-CoV-2, is regulated by upstream and intragenic elements

  PLoS Pathogens · 2023 · 20 citations

  Senior authorCorresponding

  Angiotensin-converting enzyme 2 (ACE2), part of the renin-angiotensin system (RAS), serves as an entry point for SARS-CoV-2, leading to viral proliferation in permissive cell types. Using mouse lines in which the Ace2 locus has been humanized by syntenic replacement, we show that regulation of basal and interferon induced ACE2 expression, relative expression levels of different ACE2 transcripts, and sexual dimorphism in ACE2 expression are unique to each species, differ between tissues, and are…

  PublisherOA PDFDOI

Recent grants

• NIH Grant U19AI077437

  NIH · $13.5M · 2014

• NIH Grant P01DK038108

  NIH · $15.9M · 2011

• NIH Grant P50HL042384

  NIH · $3.8M · 1998

Frequent coauthors

• Thomas M. Coffman

  Duke-NUS Medical School

  169 shared

• Matthew A. Sparks

  Georgetown University

  74 shared

• Robert Griffiths

  72 shared

• Jennifer L. Goulet

  Duke University

  59 shared

• John N. Snouwaert

  University of North Carolina at Chapel Hill

  57 shared

• Thu H. Le

  University of Rochester Medical Center

  54 shared

• Kelly Parsons

  51 shared

• Susan B. Gurley

  University of Southern California

  50 shared

Education

• Ph.D., Toxicology

  University of California, Berkeley

  1984

• M.S., Toxicology

  University of California, Berkeley

  1981

• B.S., Toxicology

  University of California, Berkeley

  1979

Similar researchers at University of North Carolina at Chapel Hill

• Paul Watkinsh-107
• Scott Randellh-100
• Alexander Tropshah-93