Baker Institute for Animal Health
235 Hungerford Hill Road
Ithaca, NY 14853
Phone: (607) 256-5635
How bioactive lipids called prostaglandins contribute to inflammation during helminth infection and allergic disease is unclear. False-colored image of hemotoxylin and eosin-stained lung tissue from mice lacking the prostaglandin D2 receptor infected with the rodent parasite Nippostrongylus brasiliensis courtesy of Dr. Elia Tait Wojno.
During helminth infection and allergy, the immune system promotes the development of a specific type of inflammation, referred to as type 2 inflammation. Type 2 inflammation is characterized by a particular set of innate and adaptive immune cell responses, which in turn cause mucin production and changes in epithelial cell physiology that lead to the signs and symptoms of helminth infection and allergic disease.
During type 2 inflammation, immune cells and non-hematopoietic cells produce factors called cytokines, which are bioactive proteins that serve as messengers. Cytokines bind to receptors found on the surface of multiple cell types, and the unique interaction of a cytokine and its receptor on a cell’s surface relays important information to that cell and directs its future activities. Thus, cytokines are key regulators of an immune response and help to determine the outcome of type 2 inflammation during helminth infection and allergy.
In addition to cytokines, immune cells also produce other factors during type 2 inflammation, including a class of bioactive lipids called prostaglandins. These molecules can be produced in great quantities during inflammation, and like cytokines, they also bind to receptors on the surface of immune cells to communicate and direct immune cell activities. However, how prostaglandins regulate immune cells is not fully understood.
The Tait Wojno laboratory is working on projects that aim to better understand how and when prostaglandins are produced, how they communicate with their target cells, and how they ultimately shape the course of a type 2 immune response during helminth infection and allergic disease. These studies will hopefully inform the development of new treatments for type 2 inflammation that block inflammatory activities of the prostaglandins.