Kevin Fuller, PhD

  • Associate Professor of Ophthalmology

Education & Training

  • Postdoctoral – Department of Molecular and Systems Biology, Dartmouth Medical School
  • PhD - Pathobiology & Molecular Medicine, University of Cincinnati College of Medicine
  • BS - Microbiology, Bowling Green State University

Research Interests

Fungi are agents devastating infections, including vision-threatening keratitis and life-threating pneumonia. Our group is interested in the pathobiology of these infections, particularly with respect to the following questions: (1) what metabolic/physical stresses do fungi encounter in during ocular versus pulmonary infection, (2) what signaling pathways allow fungi to adapt to those stresses, and (3) what host pathways contribute to disease development or regulation, and ultimately (4) can fungal or host pathways serve as novel therapeutic targets? Along with our collaborators, we are taking several approaches to these ends with an emphasis on two common mold pathogens, Aspergillus and Fusarium. First, we are analyzing patient specimens obtained from large clinical trials to determine which fungal genotypes and phenotypes correlate with disease outcome. Second, we are using systems-wide techniques (transcriptomics, proteomics) to determine the fungal and host metabolic response during infection. Various in vitro or in vivo models of infection are then used to probe the influence of candidate fungal or host genes on disease pathogenesis, as well as to determine if compounds that modulate the associated pathways can be developed as novel antifungals or anti-inflammatories that improve disease outcomes.

Publications

1) Lightfoot JD, Adams EM, Kamath MM, Wells BL, and Fuller KK (2024). Aspergillus fumigatus hypoxia adaptation is critical for the establishment of fungal keratitis. Investigative Ophthalmology and Vision Science. 65:31. PMID: 38635243.
 
2) Kamath MM, Lightfoot JD, Adams EM, Kiser RM, Wells BL, and Fuller KK. (2023) The Aspergillus fumigatus UPR is variably activated across nutrient and host environments and is critical for the establishment of corneal infection. PLOS Pathogens. 19:e1011435. PMID: 37906600.
 
3) Dos Reis TF, de Castro PA, Bastos RW, Pinzan CF, Souza PFN, Ackloo S, Hossain MA, Drewry DH, Alkhazraji S, Ibrahim AS, Jo H, Lightfoot JD, Adams EM, Fuller KK, deGrado WF, and Goldman GH. (2023) A host defense peptide mimetic, brilacidin, potentiates caspofungin antifungal activity against human pathogenic fungi. Nature Communications. 14:2052. PMID: 37045836. 
 
4) Brown ME, Montgomery ML, Kamath, MM, Nicholas S, Liu Y, Karamichos D., and Fuller KK. (2021) A novel 3D culture model of fungal keratitis to explore host-pathogen interactions within the stromal environment. Experimental Eye Research. 207:108581. PMID: 33865843.
 
5) Montgomery ML and Fuller KK. (2020) Experimental models for fungal keratitis: an overview of principles and protocols. Cells. 9: 1713. PMID: 32708830. 
 
6) Lightfoot JD and Fuller KK. (2019) CRISPR/Cas9-mediated gene replacement in the fungal keratitis pathogen Fusarium solani var. petroliphilum. Microorganisms. 16;7(10). pii: E457. PMID: 31623147.
 
7 )Hendrickson AH, Umlauf S, Choi JY, Thekkiniath J, Surovtseva YV, Fuller KK, Reynold T, Voelker, DR, and Ben Mamoun C. (2019) High-throughput screening for phosphatidylserine decarboxylase inhibitors using a distyrylbenzene-bis-aldehyde (DSB-3)-based fluorescence assay. Journal of Biochemistry. 9:12146-12156. PMID: 31227523.