Basophil-Derived Tumor Necrosis Factor Can Enhance Survival in a Sepsis Model in Mice
This week we profile a recent publication in Nature Immunology from
Dr. Adrian Piliponsky (pictured) at Seattle Children’s Research Institute.
Can you provide a brief overview of your lab’s current research focus?
My lab studies inflammatory responses involving mast cells and myeloid cells. Our goal is to understand how the body controls the immune system’s response to bacterial infections – and how this process becomes dysregulated.
Our current research focuses on the role of basophils and mast cells in the regulation of inflammation during bacterial infections. Our basophil studies indicate that these rare cells play a major role in the initiation and enhancement of the host immune response against infection and are one of the main focus of our research.
What is the significance of the findings in this publication?
Our publication in Nature Immunology revealed how a rare group of white blood cells called basophils play an important role in the immune response to a bacterial infection, preventing the development of sepsis.
Specifically, our studies showed that basophils were one of the first types of immune cell to appear at the sepsis infection site. The presence of basophils not only enhanced inflammation at the early stages of an immune response to infection and improved survival in mice, but did this in part by releasing an infection-fighting protein known as tumor necrosis factor (TNF).
Building on these findings could lead to better ways to prevent the dangerous immune response that strikes more than 30 million people worldwide every year.
What are the next steps for this research?
These studies lay the groundwork for future research projects focused on certain aspects of basophil function could offer better ways to determine an individual’s risk for sepsis or prevent the dysregulated immune response that can lead to sepsis.
This research was funded by:
Research in my lab was supported by the National Institute of Health (NIH) (R01 HL113351, R01 HL141094) and the American Heart Association (AHA) (12GRNT9680021). Other funding for the study was supported by the NIH (R01 CA72074, R37 AI23990, R01 AI070813 and R01 AR067145), and a grant from the Russian Science Foundation (14-50-00060).