Identification of Borrelia burgdorferi in the Brains of Regulatory T Cell Depleted Mice
Mentor 1
Dean Nardelli
Location
Union Wisconsin Room
Start Date
28-4-2017 1:30 PM
End Date
28-4-2017 4:00 PM
Description
Lyme disease, caused by the spirochete bacterium Borrelia burgdorferi, is a significant health concern. According to CDC data, an estimated 300,000 people are diagnosed with the disease every year. It is spread through the bite of a black legged tick infected by the bacterium, and may cause symptoms in the neurological, musculoskeletal, and cardiac systems. However, not all individuals infected by B. burgdorferi develop the symptoms of Lyme disease, suggesting that there are immune factors regulating the severity of symptoms following infection. We hypothesize that CD4+CD25+Foxp3+ regulatory T (Treg) cells prevent B. burgdorferi from entering the central nervous system (CNS). To investigate this phenomenon, our lab aims to determine how infection with B. burgdorferi will compromise the blood brain barrier of mice, allowing the spread of the bacteria into the CNS. We hypothesize that without Treg functionality, B. burgdorferi will disseminate to the brain. We intend to determine the efficiency of applying this model to measure neurological symptoms of Lyme disease, as there is currently no known model in practice at this time. Therefore, the implications of this research are essential to understanding the role of Treg cells in preventing neural symptoms of Lyme disease, a step towards preventing the disease progression, while also formulating a model of study to do further investigative research on a prominent health concern.
Identification of Borrelia burgdorferi in the Brains of Regulatory T Cell Depleted Mice
Union Wisconsin Room
Lyme disease, caused by the spirochete bacterium Borrelia burgdorferi, is a significant health concern. According to CDC data, an estimated 300,000 people are diagnosed with the disease every year. It is spread through the bite of a black legged tick infected by the bacterium, and may cause symptoms in the neurological, musculoskeletal, and cardiac systems. However, not all individuals infected by B. burgdorferi develop the symptoms of Lyme disease, suggesting that there are immune factors regulating the severity of symptoms following infection. We hypothesize that CD4+CD25+Foxp3+ regulatory T (Treg) cells prevent B. burgdorferi from entering the central nervous system (CNS). To investigate this phenomenon, our lab aims to determine how infection with B. burgdorferi will compromise the blood brain barrier of mice, allowing the spread of the bacteria into the CNS. We hypothesize that without Treg functionality, B. burgdorferi will disseminate to the brain. We intend to determine the efficiency of applying this model to measure neurological symptoms of Lyme disease, as there is currently no known model in practice at this time. Therefore, the implications of this research are essential to understanding the role of Treg cells in preventing neural symptoms of Lyme disease, a step towards preventing the disease progression, while also formulating a model of study to do further investigative research on a prominent health concern.
