March 25 – 26, 2019
Inflammation is an acute and dynamic protective response to infection, tissue injury, or surgical trauma. Complete resolution of this response and return to homeostasis is essential for restoring healthy tissues. Over the past decade it has been recognized that the resolution of inflammation involves active processes responsible for initiating inhibition of inflammatory cell recruitment and egress of inflammatory cells. The failure of inflammation resolution machinery is suspected in the development of chronic inflammation. Gaining an understanding of the principles of inflammation resolution is important in deciphering the complex process in the biology of an organ/tissue and ultimately in the pathology of inflammatory disease.
As inflammation is implicated in an array of disease conditions studied and supported by multiple NIH institutes. The focus of this Trans-NIH workshop was to gain an understanding on the state of the science in inflammation resolution biology and to develop coordinating strategies to promote this research area of shared interest across the NIH.
The workshop deliberations explored the current state of science and identify knowledge gaps including:
- What are the mediators and pathways involved in the resolution of inflammation?
- How perturbations in the resolution of acute inflammation may contribute to chronic inflammation?
- Are these pathways conserved across the organs/species?
- How do environmental agents perturb resolution and promote to development of chronic inflammation?
- Who is susceptible to development of chronic inflammation?
- What is the role of genetic and epigenetic regulators in this process?
- Ultimately, how this knowledge can be exploited for designing therapeutic or interventional strategies?