To Find Promise for Patients with Laryngotracheal Stenosis
December 2, 2016
December 2, 2016
Kevin Motz, a fourth-year resident in the Department of Otolaryngology–Head and Neck Surgery, admits that he wasn’t a particularly strong student in high school. However, when he arrived at Stevenson University for his undergraduate education, he says, members of the science faculty saw something that he didn’t see in himself.
“They invested in me,” he remembers. “They helped me unleash my true potential and realize what I was capable of.”
After completing his undergraduate degree in biology, he attended Georgetown University School of Medicine. Now at Johns Hopkins, Motz is showcasing that potential in a big way. As a recipient of one of the coveted National Institutes of Health T32 training grants as well as a CORE grant from the American Academy of Otolaryngology-Head and Neck Surgery, he is spending two years in Johns Hopkins physician-researcher Alexander Hillel’s laboratory studying the mechanisms behind laryngotracheal stenosis (LTS), a step that could lead to new, more effective treatments for this debilitating disease.
LTS is characterized by scarring and subsequent narrowing of the airway, eventually restricting breathing and hindering some patients’ ability to speak. The most common trigger is prolonged tracheal intubation, a procedure in which a tube is inserted into the airway, to help patients breathe. Other cases arise from autoimmune disorders or from no known cause.
Current treatment for this disease involves periodically dilating or stretching the airway or releasing scar tissue with a laser; however, these methods provide only temporary relief. The only permanent cure is surgery to remove the scarred portion of the airway and reconnect the healthy ends. Neither is an ideal option, Motz says.
Developing new treatments requires learning what causes patients to develop airway scarring in the first place—the focus of Hillel’s and Motz’s research. Motz is currently investigating the role of groups of immune cells known as CD4 T cells. Using mice with induced airway scarring as a model, Motz has identified increased numbers of these cells in tracheal scar tissue. Currently, he and his colleagues are working on blocking a subset of these cells known as T helper 2 cells. Preliminary evidence demonstrates that mutant mice carrying an induced genetic defect that blocks the development of these cells form significantly less airway scarring and stenosis.
Motz says he hopes that gaining a basic understanding of this disease will lead to drugs that can block the development of LTS, perhaps by blocking immune system involvement. In addition to advancing the field, these studies are also giving him a strong background to follow in the footsteps of his mentor, Hillel, who also did a T32 fellowship during his own training at Johns Hopkins.
“Kevin’s productivity in my lab has been strong,” Hillel says, “but really, it’s his growth as a clinician-scientist that has made me proud.”
After completion of his residency, Motz intends on pursuing advanced fellowship training in otolaryngology and says he looks forward to continuing his research in LTS.
For information, call 443-287-2124. Visit hopkinsmedicine.org/otolaryngology.