Department of Microbiology and Immunology
Basic Sciences Building
New York Medical College
Valhalla, NY 10595
Course Director, Foundations in Biomedical Research
Assistant Course Director, Medical Microbiology
Founding Director, Summer Trainees in Academic Research (STAR)
Executive Committee on Education and Curriculum
Education and Curriculum 1st and 2nd Year Subcommittee
Graduate Faculty Council
My laboratory studies host-pathogen interactions, with a focus on microbial mechanisms of immune evasion. The model organism used is Borrelia burgdorferi, the bacterial agent of Lyme disease. Lyme disease is the most common tick-transmitted infection in North America, and both incidence and geographical range are expanding. Current CDC estimates place the number of cases per year in the United States at over 300,000, and this number is expected to increase as the geographical range of the tick vector expands. If not promptly treated with an appropriate antibiotic, B. burgdorferi can enter the blood stream, disseminate to target tissues and cause long-term and potentially debilitating sequelae, including arthritis, carditis, and central nervous system disorders. After B. burgdorferi is deposited into the skin through the bite of a feeding tick, the majority of Lyme disease patients develop a characteristic expanding skin rash, erythema migrans, caused by an influx of immune cells recruited to the site of inoculation by the presence of the pathogen and various components of tick saliva. It is here in the skin that the bacterium first encounters host innate immune cells; the nature of the interactions with these cells may be a critical nexus that determines the outcome of infection. While many infections are eliminated in the skin, certain B. burgdorferi genotypes are more likely to evade immune defenses, enter the bloodstream, and invade target tissues that include the joints, heart, and central nervous system. Long-term sequelae--most commonly arthritis--develop in approximately 20% of patients with untreated Lyme disease.
We employ multiple approaches, including human primary immune cells, in vivo infection models, and specimens collected from Lyme disease patients, to study the mammalian immune response to B. burgdorferi. Preliminary studies indicate that strains of B. burgdorferi that are more likely to cause disease are also able to cause immune suppression of host dendritic cells, a type of innate immune cell that can skew the differentiation of T lymphocytes towards a suppressor phenotype. Current investigations utilize whole transcriptome next-generation RNA sequencing to examine the coordinate regulation of human and B. burgdorferi genes in clinical samples in order to provide a more comprehensive understanding of the complex interactions that occur during the establishment of infection.
Post Graduate Studies: Harvard Medical School
Center for Biologics Evaluation and Research, US Food and Drug Administration
Graduate Degree: Ph.D.
Graduate Degree Institution: Brown University, Providence, RI
Undergraduate Institution: Boston University, Boston, MA
Marques A, Schwartz I, Wormser GP, Wang Y, Hornung RL, Demirkale CY, Munson PJ, Turk SP, Williams C, Lee CCR, Yang J, and Petzke MM (2018). Transcriptome assessment of erythema migrans skin lesions in patients with early Lyme disease reveals predominant interferon signaling. The Journal of Infectious Diseases 2018:217:158-67.
Love AC, Schwartz I, and Petzke MM (2015). Induction of indoleamine 2,3-dioxygenase by Borrelia burgdorferi in human immune cells correlates with pathogenic potential. Journal of Leukocyte Biology 97(2):379-390. doi: 10.1189/jlb.4A0714-339R.
Petzke MM and Schwartz I (2015). Borrelia burgdorferi pathogenesis and the immune response. Clinics in Laboratory Medicine 35(4):745-764. doi: 10.1016/j.cll.2015.07.004.
Love AC, Schwartz I, and Petzke MM (2014). Borrelia burgdorferi RNA induces type I and type III interferons via TLR7 and contributes to the production of NF-κB-dependent cytokines. Infection and Immunity 82(6):2405-2416. doi:10.1128/IAI.01617-14.